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Neurology 101

Neurology for the Upper Cervical Diplomate 2012
by

Marc Lamantia

on 28 September 2016

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Transcript of Neurology 101

Marc J. Lamantia M.S.,D.C.,DACNB
Neurology 201 and 202 for the Upper Cervical Diplomate
Fundamental Concepts of Clinicial Neurology
Santiago Ramon y Cajal
Camillo Golgi 1843-1926
Charles Bell 1774-1842
Charles Scott Sherrington 1857-1952
Francios Magendie 1783–1855
The Neuron
The Neuron Theory.
Wilhelm Von Waldeyer

Named the "Neurone",
and its three parts.
1. The cell body
2. Nerve Fiber
3. Branches

Learned staining techniques from Golgi, and was
the first to recognized and ordered pattern of
connectivity (in cerebellum and the retina

Reazione Nera- The black Reaction

Supported continuous network Theory-"Reticularist"

The Synapse
The spinal Reflex
Nerve Cell doctrine

“On laying bare the roots of the spinal nerves, I found that I could cut across the posterior fasciculus of nerves, which took its origin from the posterior portion of the spinal marrow without convulsing the muscles of the back; but that on touching the anterior fasciculus with the point of the knife, the muscles of the back were immediately convulsed
Established that the posterior roots are sensory and the anterior roots motor in 1822. This clear evidence for a functional division in the central nervous system was of tremendous import, as much of the subsequent research involved pursuing this division to ever higher centres. It also provided a physiological basis for localization of function
Unipolar
Bipolar
Multipolar
Brainstem organization
Cerebellar integration
suprasegmental
Inhibition
Bell-Magendie Law
Loved Animals
Receptor activation
Genetic expression
Epigenetic changes
Reticular Theory” versus “Neuron Doctrine”
Motor Unit Potentials
3rd aspect of clinical EMG
Waveforms are analyzed in terms of latency and amplitude.
May tease out conduction defects either peripherally or centrally: peripheral nerve, plexi, root, cord, brainstem, thalamus or cortex.
May help determine if deficits are as a consequence of single or multiple. lesions or diffuse processes
SEP’s cannot give a final determination on etiology or final diagnosis.
Diagnostic utility of SEP
Mixed nerves or pure patch signature dermatomal regions are stimulated.
1st order afferent volley travels in the peripheral nerves, through the plexi and toward the cord to the posterior column ipsilaterally to synapse in nucleus cuneatus and gracillis.
2nd order neuron dessucates in midbrain to contra lateral medial leminscus to synapse on VP nucleus of thalamus.
3rd order neuron projects to ipsilateral parietal somatosensory cortex on the post central gyrus.
SEP Pathway
SEP studies capture bioelectrical activity of somatic afferents as they barrage the primary sensory cortex via the dorsal column-medial lemniscal system.
Fibers involved in generation of observed waveforms are those of sensory group 2 medium sized myelinated spindles, joint receptors and cutaneous mechanoreceptors which transmit at approximately 40-70 m/s
Distal stimulation of these fibers and the time it takes to reach predesignated pick-up sites is what is measured.
Somatosensory Evoked Potentials
Classical NCV is gold standard for verification and localization of mononeuropathy and distinguishing between mononeuropathies vs. poly-neuropathies.
Primarily used for peripheral nervous system evaluations.
Late responses, (H-reflex and Motor F-waves) may somewhat reflect the central pathway at the segmental level only.
Normality of NCV in the presence of other subjective and objective findings, directs our attention to central pathways
Applications & Rational for use of NCV
Distal Latencies
Conduction velocities
Amplitude
Studies are either
Antidromic
Orthodromic
SNAP Assessment
Isolated study of the sensory side of mixed nerves is accomplished by selectively stimulating or recording from a sensory nerve or distal sensory branch.
Responses are sensory nerve action potentials or SNAP’s.
1 stimulation site necessary and latencies reflect nerve conduction only.
Sensory NCV
Distal Latencies
Conduction velocities
Amplitudes.
CMAP Assessment
Responses from muscle after supramaximal stimulation of nerve.
The recorded potentials are called CMAP’s (compound motor unit action potentials).
NCV of motor nerve segments = d/t
The latency of the M-response is not as a result of nerve conduction only. Therefore 2 stimulation sites are used, and the calculation is based on the conduction between them.
Motor NCV
Nerve & Muscle tissue are voltage sensitive
Ionic channels can be opened by external electrical field
Clinical tests are used to evoke responses when and where it is appropriate.
Excitable Membranes
Nerve and muscle fibers can be electrically excited, depolarized by external stimuli and the responses recorded based on the change of voltages produced.
A region of depolarized membrane further depolarizes adjacent membrane creating an AP (action potential) which propagates in an all or none response.
The speed at which an AP propagates along the membranes is its conduction velocity.
Nerve Conduction Velocity
Should outline why study was done or rationale for further evaluation.
Tab data and waveforms displayed, commenting on muscles sampled and sites, insertional activity, spontaneous activity, motor unit potentials, recruitment interval and interference pattern.
Conclusion based on observations not necessarily a definitive diagnosis.
Clinical EMG Reports
Needs appropriate formulation based on clinical question not answered.
History and examination is essential.
EMG examination usually done in conjunction with or in follow-up to NCV/SSEP.
Quantitative Needle EMG performed mainly to evaluate Jitter and Blocking.
Clinical EMG Exam
Complete vs. incomplete
Indicates pathology of nerve or muscle based on pattern.
Induced by maximum volitional effort.
Interference Pattern
5th aspect of clinical EMG
High frequency trains of potentials which wax and wane like dive bomber sounds.
Fire as a consequence of muscle membrane irritability.
Seen in myotonic disorders, hyperkalemic periodic paralysis and myopathy of acid maltase deficiency.
Myotonic Discharge
Denervation potential seen later in injury, after 1 month
Observed with Fibs, and rarely seen in healthy muscle
Trains of PSW’s, and Myotonic discharge may be observed early in acute injury in the paraspinals.
Commonly seen in denervated muscle, polymyositis, trichinosis and muscular dystrophy,
Positive Sharp Waves
Activity seen in single muscle fiber.
Sign of denervation, 5-10 Hz discharge rate is pathologic.
Appear 2-4 weeks after acute neuropathic lesion in the paraspinals and longer in the extremities.
Persists until reinervation or atrophy.
Reinervation takes 8 months or sooner, at 1-3mm/day.
Seen in polymyositis, muscular dystrophy, muscle trauma, trichinosis, botulism and acid maltase deficiency
Fibrillation potentials
Seen when there is muscle membrane irritability in disorders of nerve, muscle or junctional defects.
Fibrillation potentials.
Positive sharp waves.
Fasciculation potentials.
Myotonic discharge.
Myokymic discharge.
Spontaneous Activity
2ND aspect of clinical EMG
Insertional activity
Spontaneous potentials
Motor unit potentials
Recruitment pattern
Interference pattern
Aspects of Clinical EMG
Allows for localization of lesion, either neural, muscular or junctional.
Is not pathognomonic for any disorder therefore cannot provide a definite Dx
May or may not support clinical Dx.
Used as a piece of the diagnostic puzzle in conjunction with other appropriate physiological, anatomical and clinical testing.
EMG Examination
Electronic equivalent of the monosynaptic ankle jerk reflex.
Preserved in all muscles at birth
Found in few muscles after first year of life, FCR and Gastroc-soleus.
Posterior tibial orthodromic 1A Afferent access through dorsal root with monosynaptic excitation of alpha motor neuron at ventral root of S1 level.
Lower Extremity Hoffmann Reflex
Motor nerve studies of the round trip time it takes the propagated action potential along a motor nerve antitoxic/afferent, off the anterior horn cell bodies and orthodromic/efferent to the target muscle.
Not a reflex, F stands for foot!?
Reflects motor root integrity.
Parameters to measure F-waves include persistency, latency and chronodispersion.
Motor F-waves
Stimulation is electrical DC voltage of variable amperage and duration, percutaneously, causing depolarization.
Electrodes are used for stimulation, recording and grounding
Multichannel differential amplification needed to provide variable amplification of recorded signals of different gains.
Pre-amp input is active, reference and ground
Filters used to reject noise and increase signal.
Display is 2 dimensions, time on the horizontal and voltage on the vertical.
Stimulation marks start of display across the screen. Trace deflects up or down.
Markers indicate time of onset of potential and amplitude of voltage differences.
Technical Aspects of NCV
Observed under minimal, moderate and maximal volitional contraction.
Is a graded response of smallest to largest MUP’s
Amplitude variation indicates # of units firing.
Pattern can indicate neurogenic or myogenic disorders.
Recruitment Pattern
4th aspect of clinical EMG
High frequency potentials of constant amplitude & frequency arising from muscle, spontaneously or after voluntary contraction.
Seen in: muscular dystrophy, polymyositis, chronic partial denervation, glycogen storage disease, hyperkalemic periodic paralysis and hypothyroidism.
Complex Repetitive Discharge
Spontaneous firing of entire motor unit and may be seen if occurs near surface of skin.
Classified as benign or pathologic.
Pathologic fasciculation's are generated from lower motor neuron demise and is seen with FIB’s & PSW’s
Large potentials in the range 400-800microvolts.
Commonly seen in:
Lumbar spinal stenosis, radiculopathies, anterior horn cell disease, entrapments, cervical spondylosis, Charcott-Marie tooth disease, Guillan Barre syndrome, polio, syringomyelia, tetany and thyrotoxicosis
If seen in many muscles think ALS.
Fasciculation Potentials
Normal, prolonged or decreased
Is affected differently depending on pathology present.
Denervated muscle
Poliomyelitis
Myotonic disorders
Myopathies
Atrophic disorders
Etc…
Insertional Activity
1st aspect of clinical EMG
Evaluates motor side of the nervous system
70% sensitive for radiculopathies
30% of radiculopathies affect sensory root and produce no motor signs
Determines denervation and localizes level of lesion
Needle Electromyography
Mixed nerves or pure patch signature dermatomal regions are stimulated.
1st order afferent volley travels in the peripheral nerves, through the plexi and toward the cord to the posterior column ipsilaterally to synapse in nucleus cuneatus and gracillis.
2nd order neuron dessucates in midbrain to contra lateral medial leminscus to synapse on VP nucleus of thalamus.
3rd order neuron projects to ipsilateral parietal somatosensory cortex on the post central gyrus.
SEP Pathway
SEP studies capture bioelectrical activity of somatic afferents as they barrage the primary sensory cortex via the dorsal column-medial lemniscal system.
Fibers involved in generation of observed waveforms are those of sensory group 2 medium sized myelinated spindles, joint receptors and cutaneous mechanoreceptors which transmit at approximately 40-70 m/s
Distal stimulation of these fibers and the time it takes to reach predesignated pick-up sites is what is measured.
Somatosensory Evoked Potentials
Electronic equivalent of the monosynaptic ankle jerk reflex.
Preserved in all muscles at birth
Found in few muscles after first year of life, FCR and Gastroc-soleus.
Posterior tibial orthodromic 1A Afferent access through dorsal root with monosynaptic excitation of alpha motor neuron at ventral root of S1 level.
Lower Extremity Hoffmann Reflex
Distal Latencies
Conduction velocities
Amplitude
Studies are either
Antidromic
Orthodromic
SNAP Assessment
Motor nerve studies of the round trip time it takes the propagated action potential along a motor nerve antitoxic/afferent, off the anterior horn cell bodies and orthodromic/efferent to the target muscle.
Not a reflex, F stands for foot!?
Reflects motor root integrity.
Parameters to measure F-waves include persistency, latency and chronodispersion.
Motor F-waves
Distal Latencies
Conduction velocities
Amplitudes.
CMAP Assessment
Responses from muscle after supramaximal stimulation of nerve.
The recorded potentials are called CMAP’s (compound motor unit action potentials).
NCV of motor nerve segments = d/t
The latency of the M-response is not as a result of nerve conduction only. Therefore 2 stimulation sites are used, and the calculation is based on the conduction between them.
Motor NCV
Stimulation is electrical DC voltage of variable amperage and duration, percutaneously, causing depolarization.
Electrodes are used for stimulation, recording and grounding
Multichannel differential amplification needed to provide variable amplification of recorded signals of different gains.
Pre-amp input is active, reference and ground
Filters used to reject noise and increase signal.
Display is 2 dimensions, time on the horizontal and voltage on the vertical.
Stimulation marks start of display across the screen. Trace deflects up or down.
Markers indicate time of onset of potential and amplitude of voltage differences.
Technical Aspects of NCV
Nerve and muscle fibers can be electrically excited, depolarized by external stimuli and the responses recorded based on the change of voltages produced.
A region of depolarized membrane further depolarizes adjacent membrane creating an AP (action potential) which propagates in an all or none response.
The speed at which an AP propagates along the membranes is its conduction velocity.
Nerve Conduction Velocity
Should outline why study was done or rationale for further evaluation.
Tab data and waveforms displayed, commenting on muscles sampled and sites, insertional activity, spontaneous activity, motor unit potentials, recruitment interval and interference pattern.
Conclusion based on observations not necessarily a definitive diagnosis.
Clinical EMG Reports
Complete vs. incomplete
Indicates pathology of nerve or muscle based on pattern.
Induced by maximum volitional effort.
Interference Pattern
5th aspect of clinical EMG
Observed under minimal, moderate and maximal volitional contraction.
Is a graded response of smallest to largest MUP’s
Amplitude variation indicates # of units firing.
Pattern can indicate neurogenic or myogenic disorders.
Recruitment Pattern
4th aspect of clinical EMG
Motor Unit Potentials
3rd aspect of clinical EMG
High frequency potentials of constant amplitude & frequency arising from muscle, spontaneously or after voluntary contraction.
Seen in: muscular dystrophy, polymyositis, chronic partial denervation, glycogen storage disease, hyperkalemic periodic paralysis and hypothyroidism.
Complex Repetitive Discharge
Spontaneous firing of entire motor unit and may be seen if occurs near surface of skin.
Classified as benign or pathologic.
Pathologic fasciculation's are generated from lower motor neuron demise and is seen with FIB’s & PSW’s
Large potentials in the range 400-800microvolts.
Commonly seen in:
Lumbar spinal stenosis, radiculopathies, anterior horn cell disease, entrapments, cervical spondylosis, Charcott-Marie tooth disease, Guillan Barre syndrome, polio, syringomyelia, tetany and thyrotoxicosis
If seen in many muscles think ALS.
Fasciculation Potentials
Denervation potential seen later in injury, after 1 month
Observed with Fibs, and rarely seen in healthy muscle
Trains of PSW’s, and Myotonic discharge may be observed early in acute injury in the paraspinals.
Commonly seen in denervated muscle, polymyositis, trichinosis and muscular dystrophy,
Positive Sharp Waves
Activity seen in single muscle fiber.
Sign of denervation, 5-10 Hz discharge rate is pathologic.
Appear 2-4 weeks after acute neuropathic lesion in the paraspinals and longer in the extremities.
Persists until reinervation or atrophy.
Reinervation takes 8 months or sooner, at 1-3mm/day.
Seen in polymyositis, muscular dystrophy, muscle trauma, trichinosis, botulism and acid maltase deficiency
Fibrillation potentials
Seen when there is muscle membrane irritability in disorders of nerve, muscle or junctional defects.
Fibrillation potentials.
Positive sharp waves.
Fasciculation potentials.
Myotonic discharge.
Myokymic discharge.
Spontaneous Activity
2ND aspect of clinical EMG
Insertional activity
Spontaneous potentials
Motor unit potentials
Recruitment pattern
Interference pattern
Aspects of Clinical EMG
Allows for localization of lesion, either neural, muscular or junctional.
Is not pathognomonic for any disorder therefore cannot provide a definite Dx
May or may not support clinical Dx.
Used as a piece of the diagnostic puzzle in conjunction with other appropriate physiological, anatomical and clinical testing.
EMG Examination
Needle Electromyography
Needle Electromyography
Nerve Conduction Velocity
Somatosensory and Dermatomal Evoked potentials


Marc Lamantia, DC, DACNB
EMG/NCV/SSEP Electrophysiology
Waveforms are analyzed in terms of latency and amplitude.
May tease out conduction defects either peripherally or centrally: peripheral nerve, plexi, root, cord, brainstem, thalamus or cortex.
May help determine if deficits are as a consequence of single or multiple. lesions or diffuse processes
SEP’s cannot give a final determination on etiology or final diagnosis.
Diagnostic utility of SEP
Classical NCV is gold standard for verification and localization of mononeuropathy and distinguishing between mononeuropathies vs. poly-neuropathies.
Primarily used for peripheral nervous system evaluations.
Late responses, (H-reflex and Motor F-waves) may somewhat reflect the central pathway at the segmental level only.
Normality of NCV in the presence of other subjective and objective findings, directs our attention to central pathways
Applications & Rational for use of NCV
Isolated study of the sensory side of mixed nerves is accomplished by selectively stimulating or recording from a sensory nerve or distal sensory branch.
Responses are sensory nerve action potentials or SNAP’s.
1 stimulation site necessary and latencies reflect nerve conduction only.
Sensory NCV
Nerve & Muscle tissue are voltage sensitive
Ionic channels can be opened by external electrical field
Clinical tests are used to evoke responses when and where it is appropriate.
Excitable Membranes
Needs appropriate formulation based on clinical question not answered.
History and examination is essential.
EMG examination usually done in conjunction with or in follow-up to NCV/SSEP.
Quantitative Needle EMG performed mainly to evaluate Jitter and Blocking.
Clinical EMG Exam
High frequency trains of potentials which wax and wane like dive bomber sounds.
Fire as a consequence of muscle membrane irritability.
Seen in myotonic disorders, hyperkalemic periodic paralysis and myopathy of acid maltase deficiency.
Myotonic Discharge
Normal, prolonged or decreased
Is affected differently depending on pathology present.
Denervated muscle
Poliomyelitis
Myotonic disorders
Myopathies
Atrophic disorders
Etc…
Insertional Activity
1st aspect of clinical EMG
Waveforms are analyzed in terms of latency and amplitude.
May tease out conduction defects either peripherally or centrally: peripheral nerve, plexi, root, cord, brainstem, thalamus or cortex.
May help determine if deficits are as a consequence of single or multiple. lesions or diffuse processes
SEP’s cannot give a final determination on etiology or final diagnosis.
Diagnostic utility of SEP
Mixed nerves or pure patch signature dermatomal regions are stimulated.
1st order afferent volley travels in the peripheral nerves, through the plexi and toward the cord to the posterior column ipsilaterally to synapse in nucleus cuneatus and gracillis.
2nd order neuron dessucates in midbrain to contra lateral medial leminscus to synapse on VP nucleus of thalamus.
3rd order neuron projects to ipsilateral parietal somatosensory cortex on the post central gyrus.
SEP Pathway
SEP studies capture bioelectrical activity of somatic afferents as they barrage the primary sensory cortex via the dorsal column-medial lemniscal system.
Fibers involved in generation of observed waveforms are those of sensory group 2 medium sized myelinated spindles, joint receptors and cutaneous mechanoreceptors which transmit at approximately 40-70 m/s
Distal stimulation of these fibers and the time it takes to reach predesignated pick-up sites is what is measured.
Somatosensory Evoked Potentials
Classical NCV is gold standard for verification and localization of mononeuropathy and distinguishing between mononeuropathies vs. poly-neuropathies.
Primarily used for peripheral nervous system evaluations.
Late responses, (H-reflex and Motor F-waves) may somewhat reflect the central pathway at the segmental level only.
Normality of NCV in the presence of other subjective and objective findings, directs our attention to central pathways
Applications & Rational for use of NCV
Electronic equivalent of the monosynaptic ankle jerk reflex.
Preserved in all muscles at birth
Found in few muscles after first year of life, FCR and Gastroc-soleus.
Posterior tibial orthodromic 1A Afferent access through dorsal root with monosynaptic excitation of alpha motor neuron at ventral root of S1 level.
Lower Extremity Hoffmann Reflex
Isolated study of the sensory side of mixed nerves is accomplished by selectively stimulating or recording from a sensory nerve or distal sensory branch.
Responses are sensory nerve action potentials or SNAP’s.
1 stimulation site necessary and latencies reflect nerve conduction only.
Sensory NCV
Distal Latencies
Conduction velocities
Amplitudes.
CMAP Assessment
Responses from muscle after supramaximal stimulation of nerve.
The recorded potentials are called CMAP’s (compound motor unit action potentials).
NCV of motor nerve segments = d/t
The latency of the M-response is not as a result of nerve conduction only. Therefore 2 stimulation sites are used, and the calculation is based on the conduction between them.
Motor NCV
Nerve & Muscle tissue are voltage sensitive
Ionic channels can be opened by external electrical field
Clinical tests are used to evoke responses when and where it is appropriate.
Excitable Membranes
Should outline why study was done or rationale for further evaluation.
Tab data and waveforms displayed, commenting on muscles sampled and sites, insertional activity, spontaneous activity, motor unit potentials, recruitment interval and interference pattern.
Conclusion based on observations not necessarily a definitive diagnosis.
Clinical EMG Reports
Complete vs. incomplete
Indicates pathology of nerve or muscle based on pattern.
Induced by maximum volitional effort.
Interference Pattern
5th aspect of clinical EMG
Observed under minimal, moderate and maximal contraction.
Is a graded response of smallest to largest MUP’s
Amplitude variation indicates # of units firing.
Pattern can indicate neurogenic or myogenic disorders.
Recruitment Pattern
4th aspect of clinical EMG
Motor Unit Potentials
3rd aspect of clinical EMG
High frequency potentials of constant amplitude & frequency arising from muscle, spontaneously or after voluntary contraction.
Seen in: muscular dystrophy, polymyositis, chronic partial denervation, glycogen storage disease, hyperkalemic periodic paralysis and hypothyroidism.
Complex Repetitive Discharge
High frequency trains of potentials which wax and wane like dive bomber sounds.
Fire as a consequence of muscle membrane irritability.
Seen in myotonic disorders, hyperkalemic periodic paralysis and myopathy of acid maltase deficiency.
Myotonic Discharge
Spontaneous firing of entire motor unit and may be seen if occurs near surface of skin.
Classified as benign or pathologic.
Pathologic fasciculation's are generated from lower motor neuron demise and is seen with FIB’s & PSW’s
Large potentials in the range 400-800microvolts.
Commonly seen in:
Lumbar spinal stenosis, radiculopathies, anterior horn cell disease, entrapments, cervical spondylosis, Charcott-Marie tooth disease, Guillan Barre syndrome, polio, syringomyelia, tetany and thyrotoxicosis
If seen in many muscles think ALS.
Fasciculation Potentials
Activity seen in single muscle fiber.
Sign of denervation, 5-10 Hz discharge rate is pathologic.
Appear 2-4 weeks after acute neuropathic lesion in the paraspinals and longer in the extremities.
Persists until reinervation or atrophy.
Reinervation takes 8 months or sooner, at 1-3mm/day.
Seen in polymyositis, muscular dystrophy, muscle trauma, trichinosis, botulism and acid maltase deficiency
Fibrillation potentials
Seen when there is muscle membrane irritability in disorders of nerve, muscle or junctional defects.
Fibrillation potentials.
Positive sharp waves.
Fasciculation potentials.
Myotonic discharge.
Myokymic discharge.
Spontaneous Activity
2ND aspect of clinical EMG
Normal, prolonged or decreased
Is affected differently depending on pathology present.
Denervated muscle
Poliomyelitis
Myotonic disorders
Myopathies
Atrophic disorders
Etc…
Insertional Activity
1st aspect of clinical EMG
Insertional activity
Spontaneous potentials
Motor unit potentials
Recruitment pattern
Interference pattern
Aspects of Clinical EMG
Allows for localization of lesion, either neural, muscular or junctional.
Is not pathognomonic for any disorder therefore cannot provide a definite Dx
May or may not support clinical Dx.
Used as a piece of the diagnostic puzzle in conjunction with other appropriate physiological, anatomical and clinical testing.
EMG Examination
Evaluates motor side of the nervous system
70% sensitive for radiculopathies
30% of radiculopathies affect sensory root and produce no motor signs
Determines denervation and localizes level of lesion
Needle Electromyography
Needle Electromyography
Nerve Conduction Velocity
Somatosensory and Dermatomal Evoked potentials


Marc Lamantia, DC, DACNB
EMG/NCV/SSEP Electrophysiology
Distal Latencies
Conduction velocities
Amplitude
Studies are either
Antidromic
Orthodromic
SNAP Assessment
Motor nerve studies of the round trip time it takes the propagated action potential along a motor nerve antitoxic/afferent, off the anterior horn cell bodies and orthodromic/efferent to the target muscle.
Not a reflex, F stands for foot!?
Reflects motor root integrity.
Parameters to measure F-waves include persistency, latency and chronodispersion.
Motor F-waves
Stimulation is electrical DC voltage of variable amperage and duration, percutaneously, causing depolarization.
Electrodes are used for stimulation, recording and grounding
Multichannel differential amplification needed to provide variable amplification of recorded signals of different gains.
Pre-amp input is active, reference and ground
Filters used to reject noise and increase signal.
Display is 2 dimensions, time on the horizontal and voltage on the vertical.
Stimulation marks start of display across the screen. Trace deflects up or down.
Markers indicate time of onset of potential and amplitude of voltage differences.
Technical Aspects of NCV
Nerve and muscle fibers can be electrically excited, depolarized by external stimuli and the responses recorded based on the change of voltages produced.
A region of depolarized membrane further depolarizes adjacent membrane creating an AP (action potential) which propagates in an all or none response.
The speed at which an AP propagates along the membranes is its conduction velocity.
Nerve Conduction Velocity
Needs appropriate formulation based on clinical question not answered.
History and examination is essential.
EMG examination usually done in conjunction with or in follow-up to NCV/SSEP.
Quantitative Needle EMG performed mainly to evaluate Jitter and Blocking.
Clinical EMG Exam
Denervation potential seen later in injury, after 1 month
Observed with Fibs, and rarely seen in healthy muscle
Trains of PSW’s, and Myotonic discharge may be observed early in acute injury in the paraspinals.
Commonly seen in denervated muscle, polymyositis, trichinosis and muscular dystrophy,
Positive Sharp Waves
Evaluates motor side of the nervous system
70% sensitive for radiculopathies
30% of radiculopathies affect sensory root and produce no motor signs
Determines denervation and localizes level of lesion
Needle Electromyography
Position Sense
Use toes & fingers
Patient closes eyes
Move part from straight (neutral) position into either flexion (down) or extension ( up)
Patient reports direction of movement
Sensory Examination

Cerebellar testing requires cooperative patient
Cerebellar Functions
Standing (station)
Normal foot spread vs wide vs narrow
normal width is feet directly under hips
Steady vs unsteady
Have patient move feet close together
Have patient close eyes
Worsening with eye closure is Rhomberg’s sign (sensory deficit)
Gait & Station
Causal walking & then heel to toe ( tandem)
Observe:
Stride length
Smoothness of movement
Symmetry
Steadiness during turning
Gait & Station Testing
Pin ( pain) sensation
Use safety pin or broken cotton swap stick
Ask patient to distinguish pin from opposite end of safety pin ( or your finger tip)
Identify abnormal areas and then find normal ones: distal / proximal vs dermatomal
Sensory Examination
Vibration

Significance of deficits which split the forehead or chest
Sensory Examination
Light touch
Use cotton ball
Patient closes eyes
Present stimulus & ask for response
Move from abnormal area to normal
Sensory Examination
Resting tremor : present when limb is relaxed or not in active use
Parkinson’s & related disorders
Action / postural tremor :present when body part is in sustained posture ( holding phone, newspaper)
Physiological, familial
Intention tremor: present when limb actively / quickly being moved (eating, pointing, applying makeup)
Cerebellar lesions
Tremor types
Testing for ankle clonus (4+)
Usually graded 0 to 4 +
0 no response
1+ present but slight in magnitude
2+ present, easily observable
3+ present, “don’t stand in front of pt”
4+ present, recurrent contractions (clonus)
Muscle stretch reflexes (MSR)
Reflex Nerve root
Biceps C5 & 6
Brachioradialis C5
Triceps C7
Knee ( quadriceps) L3 & 4
Ankle ( gastroc/soleus) S1
Masseter CN V
Muscle stretch reflexes

hip flexion, abduction/adduction
knee extension/flexion
ankle extension (dorsiflexion) / plantar flexion
toe extensors / flexors/ abductors
Check strength proximal to distal
Sign UMN LMN
Atrophy +/- yes
Weakness yes yes
Fasciculations no yes
Muscle tone inc dec
Reflexes inc dec
Upper versus Lower motor neuron lesions
Inspect bulk of tongue
Protrude tongue
midline vs deviation to one side
Ask to press tongue against inside of cheek
Tongue deviates to the weak side
CN XII Hypoglossal
Two divisions:
Vestibular: head motion sensing
Vertigo / nystagmus / veering gait
Cochlear:
Auditory acuity finger rustle / ticking watch
Rinne test: use tuning fork & compare perception of sound via bone and air. In a normal ear air conduction > than bone conduction.
Weber test: tuning fork on the patients forehead. Normal: patient hears sound equally in both ears. .
CN VIII Vestibulo-cochlear
Corneal reflex
afferent 5; efferent 7
Facial Nerve VII contraction
Facial Nerve VII relaxed
Relative afferent pupillary defect
Visual fields
Visual acuity
Visual fields
Pupillary light reflex
CN 2 Afferent
CN 3 Efferent
Funduscopic exam
CN II Optic nerve

Use coffee, mint, vanilla, clove


Anosmia in
head trauma
frontal lobe tumor
Parkinson’s & Alzheimer’s
CN I Olfactory nerve
Level of consciousness

Orientation

Speech & Language
Normal
Dysarthric (slurred, nasal)
Use of language in symbolic sense
Fluency, comprehension, repetition
Aphasia: expressive (Broca)/ receptive (Wernicke)
Mental Status
General

Neurological exam
Mental status
Cranial nerves
Motor exam
Cerebellar
Sensory
Station & Gait
Overview
Learn / do in organized sequence

Indiana University Department of Neurology
Neurological Examination
Foot slap: peroneal palsy / L5 radiculopathy

Spastic/scissoring: corticospinal tract lesion


Waddling: hip girdle weakness muscle diseases / dystrophy

Broad based: sensory or cerebellar

Short stepped with reduced arm swing: basal ganglia (parkinsons)


Non-organic patterns
Common Patterns of Abnormality
Temperature Sensation

Good for finding “spinal level” in cord lesions
Sensory Examination
* = most commonly performed in routine examinations
Sensory Modalities:
Light touch*
Vibration* (dorsal column)
Pin* (spinothalamic)
Temperature (spinothalamic)
Position (dorsal column)
Sensory Examination
Patient flexes hip to place heel to knee
Runs heel smoothly down the crest of tibial ( shin) to ankle
Abnormal: heel oscillates above knee & slips off shin

Cerebellar: heel to shin testing
Inspection
atrophy, hypertrophy, fasciculation
Involuntary movements
tremor, chorea, dystonia, myoclonus, myotonia
Muscle Tone (resistance to passive movement)
Hypotonia (floppy)
Hypertonia
Spasticity Clasp-knife
Rigidity (Lead pipe)
Strength (grade 0 to 5)
0/5 no contraction, 3/5 overcomes gravity, 5/5 normal
Muscle stretch reflexes (0-4+) r”
Plantar response: flexor or extensor (Babinski)
Motor Exam
Palatal elevation
Gag reflex
(sensory
& motor)
Laryngeal
function
CN IX Glossopharyngeal
& X Vagus

Taste
CN VII -Facial nerve
Sensory to face and anterior scalp
Blink reflex
Motor to muscles of mastication (masseter/temporalis)
Test 3 divisions with cotton & pin
Jaw jerk reflex
CN V Trigeminal
Medial Longitudinal Fasciculus ( MLF) Lesion
INO (Internuclear ophthalmoplegia)
Third nerve palsy
Eye is “down and out”
Pupil abnormal
Compression by uncal herniation or
P-com aneurysm
Pupil normal
Nerve infarction
CN III—lesion causes eye motility problems, ptosis and mydriasis (enlarged pupil)
Are the eyes conjugate
Puplliary function
Evaluate motility
Horizontal
Vertical
Oblique
Disorders
Nerve ( nucleus)
Intra-nuclear
Supra-nuclear
CN III (oculomotor), IV (trochlear),
VI (abducens)
Fundoscopy (ophthalmoscope)
Optic disk ( optic nerve head)
Retinal vessels
Retina
Direct and consensual
Observe pupil size ( mm)
Shine light into eye from off center
Observe for pupillary constriction in stimulated & opposite eye
Accomodation
As pt looks at close target; eyes converge and pupils constrict
Pupillary light reflex
Visual acuity

VA is last line read correctly
Visual acuity
Functions:
Data acquisition & transmission
Camera control
Eye lids
Eye movements
Focus
Optic System: Overview
Parietal Functions
Mental Status
Guy in movie Airplane with the “drinking problem”
Pattern of dysfunction:
Actions break into jerky steps
Target may be missed (dysmetria)
Cerebellar: finger to nose
Patient extends finger out to your finger
Then moves finger back to nose
The back to your finger
Repeat with your finger in different position
Cerebellar: finger-nose finger
Other superficial reflexes
Stroke anterior
abdominal skin
toward umbilicus

Rectus muscles
Contract in quadrant
stimulated
Superficial Abdominal Reflex
SCM--Right SCM turns head to the left
Trapezius
Raise shoulders
CN XI -- Spinal Accessory
Left hypertropia
Right head tilt….What about the doll’s eyes?
Left IV nerve palsy
CN III (Oculomotor nerve)
Superior rectus:
elevation when the eye is aBducted
Inferior rectus:
depression when the eye is aBducted
Medial rectus: aDduction
Inferior oblique:
elevation when the eye is aDducted
CN IV (Trochlear nerve)
Superior oblique:
depression when the eye is aDducted
CN VI (Abducens nerve)
Lateral rectus: aBduction
Extraocular muscles and their actions
Toe flexion is normal. Toe extension is abnormal ( Babinski sign)
Plantar reflex
Calf muscle hypertrophy
Atrophy of intrinsic hand muscles
Motor Exam
Papilledema
Normal
CN II Optic Nerve
J Neurol Neurosurg Psychiatry
Neurological education
Editorial
Is clinical neurology really so difficult?
F Schon1, P Hart2, C Fernandez3
1Neurology Department, Atkinson Morley's Hospital, Copse Hill, London SW20 0NE, UK
Neurosciences need to be made more accessible for medical students
Neurology, it seems, has a reputation among medical specialties of being particularly difficult. This was highlighted in the British Medical Journal in 19991 when the editor wrote, “the neurologist is one of the great archetypes: a brilliant, forgetful man with a bulging cranium....who....talks with ease about bits of the brain you'd forgotten existed, adores diagnosis and rare syndromes, and—most importantly—never bothers about treatment.” The relevance of this view to the teaching of neurology was analysed in a not totally serious letter in 1994 by Ralph Jozefowicz2 entitled “Neurophobia,” in which the author claimed 50% of medical students at some stage have “ a fear of neural sciences and clinical neurology.” His explanation for this was students' inability to apply knowledge of basic sciences to the clinical situation. This letter was based on personal views not supported by what the BMJ called “evidence based education” in another editorial in 1999.3 We therefore set out to ascertain perceptions of seven major medical specialties among British medical students, senior house officers (SHOs), and general practitioners, principally in order to find out the actual perceptions of neurology in comparison with the other disciplines.
©2002 by BMJ Publishing Group Ltd
Schon F et al. J Neurol Neurosurg Psychiatry 2002;72:557-559
Histograms showing questionnaire results on seven medical disciplines.

The Post Doctoral learner desires independence and is self-motivated, therefore I beleive an androgogic approach this weekend will serve you best. It will require you to further your own self study in each topic of discussion and to apply it clinically to attain the greatest benefit from you attendence.
volitional
Cranial Nerves
Clinical Neuroscience
Objectives / Outline
The epigenome is particularly susceptible to disruption during gestation, neonatal, puberty and old age (Feinberg 2007)
Epigenetics and epigenomic medicine encompass a new science of brain and behavior that are already
providing unique insights into the mechanisms underlying brain development, evolution, neuronal
and network plasticity and homeostasis, senescence, the etiology of diverse neurological diseases
and neural regenerative processes.
Epigenetic mechanisms include DNA methylation, histone
modifications, nucleosome repositioning, higher-order chromatin remodeling, non-coding RNAs,
and RNA and DNA editing.
What is Cholenergic supersensitity?
1) Medial Somatic Motor column: dealing with the midline muscles. It stretches the length of the spinal cord and much of the brainstem;
2) Lateral Somatic Motor Column: deals with the more lateral muscles which shunt or move the extremities: hence the discontinuity of this column;
3) General Visceromotor Column: these are basically the preganglionics of the cord. They are a bit more dispersed and complicated in the brainstem. This is the most visible part of the IML
Bilateral Mydriasis (pupilary constiction) due to medications with binocular vision in room light.
Ocular spasms without vision
Positive findings
The Pan Opthalmoscope
Intracranial and peripheral Pulse oximeters
Video electronystagmography
Posturography
Maddox rod
Convergence and Divergence test
Some equipment you should know about
Flashed a light at the throat and had him say AHHH.
Flashed a light at the nasal retina and watched both eyes
I covered one eye with my hand, then alternated between the two eyes.
I skillfully tapped his thenar prominence bilaterally
I had him follow my finger with his eyes only
I had him resist me to test his strength- hands and hips
I jerked his ankle and tapped his knee
7 Things I did
Mini mental exam
Obervations of head position in relation to the thorax
Pupil position and size
eyelids
Facial tone

Interview and Observations
Vertigo is considered a sensory mismatch and my involve the:
Vestibular apparatus in the inner ear
The nerves growing from the brain stem
The nuclei living in the brainstem
The extraocular eye muscles and stabilization of targets on the fovea
Proprioception loss
Intermediolateral Cell column S2-S4
Synapse on the rectum and genitals
Either the parasympathetics get released from inhibition, or they receive excitatory input? Which is it?
Sacral parasympatehtics
When I inhibit my IML, Parasympathetics can come to threshold
Look at urination
Bladder stretches- should urinate immediately
But the brain inhibits the sympathetics
Most of use can think a thought like, “now I shall pee”, and you can
Sympathics cause retention
Parasympathic dominace gives you urgency
IML inhibits Sacral parasympathetics
Do 4 things
1. Inhibit the Intermediolateral (IML) Cell Column
When you raise a limb you get sensory feedback from the periphery which activates the IML
Everything activates the IML accept
Descending pontomedulary system
Cortex
2. Facilitates gamma motor neuron
3. Dampens pain in dorsal horn (descending analgesic pathways
4. Inhibits vhc of flexors above t6 and extensors below t6.
Pontine and Medullary Reticular Pathways
Marie Charcot Tooth Disease- Hi arching feet and palate
Friedricks Ataxia
Spinocerebellar Ataxia
Hereditary Neuropathy
Plexopathies
Learn the brachial plexus presentations
Which nerve roots affect what muscle groups
Polyneuropathies
Diabetic polyneuropathy
Alcohol induced polyneuropathy
F waves will give us feedback about the proximal part of the peripheral nerve and dorsal ganglia.
Peripheral Neurology
The Postural Spondylogenic Reflex Syndrome:
The clinical symptom of pain in muscles and other soft tissues (spontaneous or elicited by palpatory pressure) has been termed the Spondylogenic Reflex Syndrome by Sutter (1974,1975).
Myotendinoses has been in observe the various systematic response to an articular/somatic dysfunction involving the individual apophyseal, occipito-atlanto-axial, and sacroiliac joints.
“Many systematic myotendinoses improve during the course of therapeutic intervention in the individual patients”.
It was therefore assumed that, in addition to other helpful physical and therapeutic procedures, the mechanical and functional correction of the spinal motion unit, according to Schmorl and Junghanns (1968), can play a significant role, if not the most crucial role in treatment.
The Postural Spondylogenic Reflex Syndrome: Clinical Correlation with Reflexes Linked to Nociceptors and Mechanoreceptors
Special Senses
Magnesium does it to, this is where drugs attempt to help
Or at the Neurotransmitter
Ca channel blockers
Define Long term Depression
Define the Hebbian Process
Kinase leads to the Gene getting turned on after transcription of protein.
Then the cell can make 2nd messenger ions (N.T.)
This is called Long Term Potentiation because the cell infrastructure is in place.
This can change if I stop using ADP
Can lead to neural degeneration.
5th Messenger- the protein
1. Neurotransmitter
2. carrier
3. Kinase
4. phosphoprotein in the Nucleus
Gene response of early genes goes on for hours to days
So when you activate this 4 Mess. pathway you strenghten pathways.
Epigentics are a 4 messenger system
Disease of mitochondria? Then activation would drive the disease further- PT 3x a week, 80 adjustments a year?
Genetic Synaptic Disease
Neurotransmitter imbalance
Adrenal and renal pathology
Creatinine, albuman, GFR, U.A.
Kidney disease = Bad Brain
Electrolyte imbalance
Big picture
You can have dysfunction at any of these structures
You can have mutation of protein, the higher probability of SNPs- EPIGENTIC FALTS
Transport system can breakdown
Carrier protein transports across the cell (requires energery)
Microtubules can transported on carrier proteins as well
Cell becomes more efficent and now more synaptic success.
Then growth factors get exchanged, through retrograde Flow
This is how neural networks work as a SYMPHONY
Neurons, glial cells, oligodentracyts, astrocyte.
Glial Cells release pro and anti imflammatory cytokines. These cells are primed over time to become over sensitive.
This can lead to chronic encephalopathy
Autoimmunity, destruction of oligodendrocyte.
This is neurodegenerative disease
Can get the aceytlcholine through because intracellular architecture breaks down (cholenergic system damaged)
Alzhemers (bradykinesis without tremor)
Parkinsonian- tauopathy causes tremor, anosmia, falls, dementia,
SNP-with tremor
Neurons and glial Cells
Midline structures (reticular formation)- they fire up to activate the frontal brain
Acetylcholine and dopamine (best friends) in the b.g. (ventral mesenscephalon)
Control of eyes, collicular maps, holds head up, postural tone- this helps
develop chewing (trigeminal nucleus- that’s whys its separate, it comes first, then CN7,9,10 function become important and are bourne out of necessity.
Ocular control (horizontal and vertical optokinetics develop)
Then they start using limbs to direct food for chewing and away they go.
The more lateral columns are regulated by the brain after it takes in the midline column information
Homologus columns
Activation causes genetic transcription for a protein
Nucleus gets activate (top of the food chain)
E.R. and Golgi apparratus builds protein
Ships to transport system to different parts of the nucleus
Midochondria is power station
Stability of Cell is dependent upon neuron function
Epilepsy, autoimmune breakdown, neuron degeneration, damage from ischemia….
The Neuron
The Neuron
Neurogensis
Commissures make use of the lamina terminales.
The first to appear is the anterior commissure.
The second is the hippocampal or fornix commissure.
By the tenth week the corpus callosum develops; it begins as a small bundle through the lamina terminales and as a result of the expansion of the neopallium it extends first anteriorly and then posteriorly, arching over the thin roof of the diencephalon.
There are three other commissures: the posterior commissure, the habenular commissure, and the optic chiasma.
Immediately above the choroidal fissure, the wall of the hemisphere thickens to form the hippocampus
The metencephalon has similar organization of the alar and basal groups of nuclei.
The marginal layers of the basal plates expand to accommodate fibers connecting the cerebral and cerebellar cortices with the spinal cord thus forming the pons
Cells from the alar plates migrate to form the pontine nuclei.
Mylination at the periphery via Schwann cells occurs at the beginning of the fourth month of development.
Central mylination via oligodendroglial cells occurs from the fourth month in-utero to the first postnatal year
During the fourth week of development, axons of neurons in the basal plate break through the marginal layer to form the ventral motor root (A).
Axons of neurons in the alar plate penetrate the marginal layer and ascend or descend to form association neurons.
Dorsal root ganglion neurons grow centrally and peripherally (B).
Dorsal nerve roots are collections of fibers originating from neurons in the dorsal root ganglion.
Distal processes join the ventral motor root to give rise to the spinal nerves.
Neuroblast are round and apolar when they migrate to the marginal layer (A).
These then differentiate into bipolar neurons (B) with one of the processes becoming a primitive axon and the other the primitive dendrites (C).
Ventral thickening results in the formation of the basal plates (A).
These contain the ventral motor horn cells.
Dorsal thickening results in the alar plates (A).
The boundary between the basal and alar plates is the sulcus limitans (A).
Neither the dorsal or ventral midline portions of the neural tube contain neuroblasts and are known as the roof and floor plates, respectively (A).
An intermediate zone of neurons (B) contain the sympathetic portion of the ANS and are located in the thoracic and upper lumbar (L2 or L#) of the spinal cord (B).
Mouse spinal cord at a similar age to A (SG, spinal ganglion).
On the periphery of the neuroepithelial layer, differentiating neuroblasts are observed.
These form the mantle layer which gives rise to the gray matter of the spinal cord.
The outermost layer of the spinal cord is known as the marginal layer.
These contain nerve fibers emerging from the neuroblasts in the mantle layer.
Subsequent myelination results in the formation of the white matter of the spinal cord.
At 5 weeks old, the prosencephalon consists of two parts:
Telencephalon (T)
Diencephalon (D) noted by the outgrowth of the optic vesicles (o).
A deep furrow, the rhombencephalic isthmus, separates the mesencephalon from the rhombencephalon (arrow).
The rhombencephalon also consists of two parts:
Metencephalon (Mt) which later forms the pons and cerebelum
Myelencephalon (My)
The metencephalon and the myelencephalon are divided by the pontine flexure.
Fusion of the neural tube begins in the cervical region and proceeds in cephalic and caudal directions (A).
Fusion is temporarily delayed at the poles creating a cranial and caudal neuropore (B). These close at the 25th and 27th day, respectively.
A mouse embryo is shown in C (similar developmental age to A).
Formation of the neural groove, neural tube, and the neural crest (A-D).
Neural crest cells go on to develop into spinal and cranial sensory ganglia.
A mouse embryo is shown in E (similar developmental age to D).
Oxidative Phosphorolation
Methylation Errors can lead to transcription errors
Bilipid membrane destruction
Wallarian Degeneration.
Neuron Degeneration
Things that talk to the brain through the thalamus (relay nuclei to the brain)
The gut
The joints
The skin
The special senses
The brain itself
Brain Function
ALL SENSORY INPUTS Summate in the Brainstem to activate the cortex
All Somatic sensory nerves terminate on the Nucleus Tractus Solitarius (NTS)
Facial Afferents summate on the Trigeminal nucleus
and the cortex activates itself.
Brain Function
The health and function of the brain is dependent upon 3 things
Glucose
Oxygen
Activation
From the
Olfaction,
the brainstem reticular formation
thalamus.
Neurology for the Upper Cervical Diplomate
Descending Pattern
Not long track signs- grey matter lesions!
Loss of pain and temperature because these pathways cross ventral to the central canal
Shawl like distribution due to more lateral aspects of the body are represented in the midline
Intrinsic lesions like a Syrinx
Intrinsic- Ventral horn disease, M.S., Infection, metabolic
Trunk, arm, Leg
Extrinsic- (ascending pattern)
disc spondyosis, tumor
- Pain and temp of the Leg FIRST, Arm, then Trunk
Dorsal columns of the upper extremity aslo affected but before the legs
Due to laminar distribution in long tract pathways.
Intrinsic vs Extrinsic Lesions
Transient unilateral mydiasis has been reported in basilar aneurysm- Walsh and Hoyt 1985
Above has also been reported in Arterial malformations, neuromas and aneurysms but typically comes with other signs of 3rd nerve palsy.
Ciliary ganglion damage results in Tonic pupil.

Oculosympathetic spasms observable upon vision denial.
CN III
CN V
CN IIX
CN IX and X














Accomodation/Pupillary to light
Corneal Reflex
Vestibuloocular
Gag
Reflexogenic systems can give real time feedback about the health of a pool of neurons.
Typically the first pass is indicative of the resting state of the system.
(Just like in cerebellar tests of acurracy )
Brain Stem Reflexes
A 50 yo Male, writer, previously treated with antipsycchotic medication, has long standing Vertigo and continued pyschiatric dysfunction.
CASE PRESENTATION- GMr
Brainstem and sacral divisions
Brainstem nucluei include
CN III superior colliculus andedinger westfall nucleus
CN VII Pontine tegmentum, ssn and lacrimal nuclei
CN IX Inferior Salavatory nucleus in rostral medulla
CNX Nucleus Ambiguous and DMNV
Parasympathetics
Close to the attachment of the dentate ligaments.
Responsible for conveying pain and temperature into the neuroaxis.
Mechanical irritation and/or ischemic compromise to the spinothalamic tracts possibly explains particular cases of severe low back and leg pain being caused by an upper cervical subluxation.
The Spinothalamic Tracts
The spinocerebellar tracts lie along the lateral edge of the spinal cord (the most probable site of maximal mechanical irritation by the dentate ligaments).
Proprioceptive tracts, which regulates muscle tone and joint position sense.
Irritation of these tracts could lead to muscle tone imbalance of the pelvic girdle resulting in a functional short leg.
The Spinocerebellar tracts
Ascending Pattern (leg is worse than arm)
Descending Pattern
Intrinsic vs. extrinsic
Sensory Dissociated – Anteriolateral system (pain and temp from opposite side, Dorsal columns ipsilaterally, light touch and vibration)
Long Tract Pattern
Doesn’t follow the
Nerve root, dermatome
Myelopathic Lesion
Vascularity
Anterior Spinal artery 2/3
Posterior Spinal artery 1/3 Dorsal horns
Spinal Cord
Do you know what nerves exit at what foramen. C6 exits at C5/C6
What about L5/S1- L5
Gluteal muscles are spared in Sciatic nerve lesions
Gastroc and Glute together have to be nerve root
What about OCC/C1?
Brachial Plexus- if it’s the finger only its at the wrist.
Entrapment syndromes
Thoracic outlet Syndromes
Peripheral neurology not our clinical focus.
Graded and indicate likelihood of good prognosis. (1-5)
Sunderland Classification of peripheral nerve damage.
Neuropraxia is reversible
Axonmesis or Neuromesis leads to problems like sphincter loss and are not reversible
Any and all peripheral nerve dysfunction has a central consequence.
The Take Away
Neuropraxia= neural conduction signal block
Axontmesis- transection of the axon
Compression or trauma
Neurotmesis- Perineum severed.
Permancy of symptoms
Denervation, muscle fibrosis
Types of peripheral nerve damage
Axon loss is sensory before motor
If Motor is affected first its usually myelin
Conduction is slow in meylin damage
NCV small- Amplitude depressions are from Axon
Axon death leads to muscle changing where acetylcholine receptors are.
Moves them to the surface to get mor activation
N.T. makes the muscle spontaneously fire
THIS IS FACICULATION- (DENERVATION Fibs and Sharps)
Peripheral Neuropathy
The nociceptive stimulation can be inhibited presynaptically when there is sufficient stimulation of the mechanoreceptors, mainly the type II receptors.
This may occur by release of endorphins: cells in the gelatinous substance of the dorsal horns.
Therefore, it would plausible to propose that these and probably other related neurophysiologic mechanisms may play at least as important a role in manual therapeutic treatment as the pure mechanical correction of one or several segmental dysfunctions.
The Postural Spondylogenic Reflex Syndrome:
The absence of pain does not automatically mean lack of soft-tissue findings.
It is well known that localized palpable muscle bands or systematic myotendinoses can be elicited upon careful palpation in many individuals who have no subjective pain complaints.
This situation is to be considered pathologic and correlates with the latent state of intervertebral insufficiency according to Schmorl and Junghanns (1968).
This could be explained on the basis of the tonic reflexogenic influence of the type 1 mechanoreceptors upon the motor neurons of the axial or peripheral musculature.
It has been shown that pain-inducing nociceptors have significantly higher thresholds than pain-inhibiting mechanoreceptors. This may explain the delay with which the individual may perceive his or her pain.
The Postural Spondylogenic Reflex Syndrome:
Type I: provide important information about joint position as they signal the angle of the articulation throughout the range of motion.
Type II: Have a low threshold and rapidly adapt to a stimulus. Detect rate of movement at the articulation.
Type III: High threshold and slowly adapting receptors. They are stimulated only at the extremes of joint movement. Structurally similar to the Golgi tendon organ of the muscular system
Type IV: Nociceptors; have a high threshold and do not adapt. These pain receptors tend to be free nerve endings.
Mechanoreceptors
Joint Mechanoreceptors
Muscle Spindle
Neuromuscular junction
Vision
Sound
Chemotactic
Baroreceptors
Olfactory
Nociceptors
Parcinian, meisners, Ruffini, Vestibular apparatus, Taste
Conduction- things stuck in your ear.
Senserineural- from the cochlea to the brain
Receptors - what processes can affet their function
MRI, CSF
Symptoms are varied
May have afferent pupillary defect
Multiple Sclerosis
Infectious disease can do the same
Neurosyphylis
Herpes leads to 20 percent increase in Alzhemiers
Can you see how peripheral nerve dysfunction has central consequences
NMDA receptor is regulating Ca,
Activated by Neurtrophic factors
Dysregulation of Ca channels
Ca degrades Phosopholipid bilayer (free radicals (phospholipase)
Causes Mitochondria to uncouple
Intracellualar calicium is the major factor for neurodegeneration
Initiates tangles and tells other NMDA channels to open
Mitochondria triggers the Ca imbalance
Read about Molecular Neurodegeneration
Apoptotic pathways
Alzhemiers (amyloid and Tau)
Dementia (Lewy bodies)
Parkisons ( A synuclein pathology)
Prions- infections disease does the same.
Corticobasilar degeneration (tau pathology)
They all are epigentic protein MUTANTS
You are what you are because of where you are in the brain. One cause. . .
Degenerative Disorders
With acivation comes fatigue.
Can be seen in the eyes
If it’s a horizontal diplopia without pupil or lid disfunction its CN 6
Its its in the vertical plane without pupil or lid involvement, its CN4 and resultant head tilt.
If its vertical with Pupil and lid- CN3
Happens post synaptically
Lambert Eaton syndrome is the same thing at the pre synapes, (Nerve gas does this)
Myesthina gravis- post synaptic antiodies block the cleft transmission
Free radical damage (Nitric Oxide)
Causes interleukin cytokines to cause inflammation leading to Na imbalance= Apoptic Neuron.
This perpetuates itself
Can be perpetuated by hypoxia (Ischemic STROKE)
Ischemic stroke gives you 4 hours to get to the hospital for good emergency outcomes.
Clot busters if ischemic
Intracellular calcium is the
MSG and Aspartame should be a dietary restricted.
This can be happening in the
Limbic system- Schizophrenia
Mesencephalon- Parkinson disease
IF YOU manipulate these people you will drive the system to crash, these patients need less activation.
Oh by the way
Sodium rushes in
Potasium moves out
Net charge goes down
Lead to hyperpolarization and refraction
This is the thing, Na and Potasium need help getting back
A pump is required
If the top dog is tired, he may not help get ya back
This leads to a swollen cell
Resting membrane potential gets closer to threshold
Spontaneous activity.
ADP and P can’t get used to make ATP
P break down the membrane and open NMDA recpetors
NMDA receptor gets activated by peripheral system- This is what reciprorcally causes the gene respone
This lets calcium into the cell and attacks the nucleus when no activation occurs.
This causes protein degradation
Mitochondrial damage
Excytotoxic cells (glutamate mediated)Neurodegenerative disease.
Action potential
Dentritic zone- reception
Somatic zone- Soma- integration of chemical encoding
Axon Hillock- Electrical impulse
This creates a gene response at the target nucleus to produce protein.
Cytokines and Neutransmitters (start as monoamine then Decarboxylase etc)
The golgi take it package it for the E.R. and off ya go to a secretory vessicle then
Lysosomes break it down
Neuron
Continuous growth of the cerebral hemispheres in the anterior, dorsal, and inferior directions result in formation of the frontal, temporal, and occipital lobes respectively (B).
Growth in the region over the corpus striatum slows resulting in overgrowth of the insula.
Craniopharyngiomas arise from remnants of Rathke’s pouch. They usually lie above the sella and may cause hydrocephalus and pituatary dysfunction
The hypophysis develops from fusion of Rathke’s pouch and the infundibulum (A, six week old embryo).
Development at 11 weeks (B).
At 16 weeks, the pars tuberalis and pars intermedia appear (C).
EM at high magnification that is developmentally similar to A (C) (arrow, Rathke’s pouch; arrow heads, infundibulum)
Mesencephalon
The basal plates consist of two groups of motor nuclei (III/IV and n. of Edinger-Westphal) (B).
The marginal layers of the basal plate enlarge and form the crus cereebri.
A transverse groove forms along the alar plates to delineate the superior and inferior colliculi.
The cerebellar plate contains neuroepithelium, marginal and mantle layers (1A).
The neuroepithelium migrate to the surface of the cerebellum to form the external granular layer (1B) which gives rise to the granule cells (2A).
Basket and stellate cells derive from proliferating cells in the cerebellar white matter
The rhombic lips, as a result of deepening of the pontine flexure, compress and form the cerebellar plate (A).
The flocculonodular lobe appears at 20 weeks of development (B) and phylogenetically the oldest part of the cerebellum.
Early stage of mouse cerebellum at similar developmental age to A where the cerebellar primordium (C, white arrow) and choroid plexus (D, black arrow) are demonstrated.
The lateral walls of the mylencephalon are everted (A).
Position of alar and basal plates in the mylencephalon at different stages of development (B and C).
Cells of the alar plate migrate to form the olivary nuclei (arrows).
The basal plate contains the motor nuclei and the alar plate contains the sensory relay nuclei (C).
The roof plate of the myelecephalon contains a single layer of ependymal cells covered by vascular mesenchyme together known as the tele choroidea. The tuft like invaginations are the choroid plexus.
Example of a patient with meningomyelocele (A).
Example of patient with rachischisis (B).
Third month of development (A).
End of fifth month of development (B).
Birth (C), the dura (and subarachnoid space) remains attached to the vertebral column at the coccygeal level.
A threadlike extension of the pia matter forms the filum terminale
Neural crest cells, in addition to developing into dorsal root neurons of the spinal and cranial sensory ganglia, they differentiate into:
sympathetic neuroblasts
Schwann cells
pigment cells
odontoblasts
meninges
mesechyme of the pharygeal arches
Gliabasts are formed by epithelial cells after the production of neuroblasts ceases.
These migrate from the epithelial layer into the mantle and marginal layers and form protoplasmic and fibbrillar astrocytes.
Oligodendroglia may be produced from gliablasts and inhabit the marginal layer.
When neuroblast and gliablast formation ceases, neuroepithelial cells differentiate in ependymal cells to line the central canal of the spinal cord.
Microglia are produced from mesenchymal cells.
Spinal cord
The wall of the closed neural tube consist of neuroepithelial cells.
These are arranged in psuedostratified epithelium and extend over the full width of the wall.
Dividing neuroepithelial cells are located at the lumen side of the tube.
The lumen of the mesencephalon connects the third and fourth ventricles and is known as the aqueduct of Sylvius (arrowheads show the roof of the fourth ventricle)
The lateral ventricles and the third ventricles communicate via the intraventricular foramen of Munro.
The lumen of the spinal cord is continuous with the brain vesicles.
The cavity of the rhombencephalon is the fourth ventricle.
The cavity of the diencephalon is the third ventricle.
The cavities of the cerebral hemispheres of the telencephalon are the lateral ventricles.
Sagittal view through a mouse embryo is shown.
At the 27th day, the cephalic end has 3 dilatations:
Prosencephalon (forebrain, F)
Mesencephalon (midbrain, M)
Rhombencephalon (hindbrain, H)
Two flexures are also formed:
The cervical flexure between H and the spinal cord
The cephalic flexure in the midbrain region
Early development
CNS begins in 3rd week with thickening of ectoderm to form the neural plate (A, dorsal view) rostral to the primitive pit.
The lateral edges then elevate to form the neural groove (B).
A mouse embryo is shown in C (similar developmental age).
CN III, IV,VI and the VHC
CN VII
CN
Clinical Homologes
Rules from Embryology
Ventral is motor
Dorsal is Sensory
If a motor tract is in the dorsal lateral aspect of the cord it deccusated! (LCST)
Same is true for Ventral Spinocerebellar tract
Anteriolateral Ascending Systems.
Cross or not?
Alar or Basilar plate?
Alar and Basilar plates
NMJ
Entrapment
Metabolic
Sensory before motor
Epineurium with bundles of nerves covered with perineurium and endoneurium
Epineurium is protective
Perineurium protects against stretch
Vasculature is also present and is suseptiple to compression (leg fall asleep)
Peripheral Nerve Damage
Climbs the Glial Fiber
Neural Migration
Telencephalon
Consists of two lateral outpocketings, the cerebral hemispheres, and a medial portion, the lamina terminales.
By the second month, the basal part of the hemispheres bulges into the lumen of the lateral ventricles to form the corpus striatum. It is divided into the caudate nucleus and the lentiform nucleus by the passage of the internal capsule fibers (B).
The choroid plexus forms at the medial attachment of the hemispheres to the roof of the diencephalon (B).
Diencephalon
The diencephalon consists of a roof plate and two alar plates but lacks a floor plate and basal plates.
A groove in the alar plates, the hypothalamic sulcus, divides the thalamus from the hypothalamus (A).
The roof plate of the diencephalon gives rise to the choroid plexus (B) and the pineal body at it’s most caudal aspect.
The figure shows the brain vesicles in an 8 week old embryo with the roof of the rhombencephalon removed.
Rhombencephalon
Myelenchephalon gives rise to the medulla oblongata.
All cranial nerves arise except I-III arise from the rhombencephalon
Spina bifida occulta occurs in 10% of healthy people and is situated from L4 to S1 (A).
Spina bifida cystica is when meninges (B) and/or neural tissue protrudes (C) through the bifid defect. These are usually not associated with mental retardation. Arnold-Chiari malformation is virtually always present.
Occasionally the neural folds do not elevate but remain as flattened masses (D and E). Associated hydrocephalus due to cord tethering and pull of cerebellum into foramen magnum.
Neural tube defects
Defects of the spinal cord resulting from abnormal closure occur in the third and fourth weeks of development.
Spina bifida is the splitting of the vertebral arches.
The incidence of severe neural tube defects is 1/1000 births.
Helps us understand the nervous system
Homologues
Longitudinal 3 dimensional understanding of N.S.
Not cross sectional.
Chiropractors activate suprasegmental structures via receptor systems or environmental change of the spinal cord or brainstem
Which leads to changes in regulation of these same homologues columns, which have affects segmentally
And of course the neuron drives this process, that bring us understanding the process of Synaptic Transmission of the Neuron
Why Embryology is important
Pyramidal
Extra Pyramidal (non volitional)
Renshaw cell- actively inhibits the VHC to keep it healthy.
Motor Pathways
Median
axillary
Musculocutane
radial
Ulnar
5
6
7
8
1
Tricks to draw Brachial Plexus 3333
If it were nerve roots would it be the entire hand? NO
Dermatomal vs. Plexus, vs. cord
Example text
Example text
Intrinsic muscles of the hand
Ventral Horn Disease
Poximal Muscles usually Primary muscle disease
Spaticity vs. weakness
FLOWCHART
FLOWCHART
No
Methylation errors
Bilipid membrane breakdown (Omega 3 F.A.)
Neuron Dysfunction
Medication,
Oxidative phosphoralation
Neurons grow on Glial Ladders, they compete, connect and activate through synaptogensis.
Hard wiring is driven by functional activation in the fetus
FLOWCHART
Migration
differentiation
Neurophysiological consiquence
Physical distress to tissues
Neurogensis
Structural subluxation
W/o atrophy, weakens with activity
Peripheral Nerve
Neuro
muscle junction
Primary Motor disease
FLOWCHART
VHC
Yes
Weakness, proximal vs distal, Faciculations, atrophy, Sensory?
Proximal Muscle weakness
Distal muscle weakness
Neurons grow on Glial Ladders, they compete, connect and activate through synaptogensis.
Stem Cell
Neurogensis
Migration
differentiation
Neurophysiological consiquence
Physical distress to tissues
Selection, competition then dentrictic
Neurogensis
Structural subluxation
Example text
This is an example text
Example text
This is an example text
Example text
This is an example text
Sleep Apnea, Palatal weakness,
Example text
This is an example text
Your Gut dysfunction will destroy the brain
Repiratory asdiosis
Thyroid Disease
Dysglycemia
Anemia
Metabolic conditions create irritability
No
Understand what can affect neurological function
Loose inhition of Embryologic flexors in axial musculature
BRAIN
No
No
No
Bad Cognitive
Loose inhition of Autonomic/gut dysfunction
Pain isnt inhibited
FLOWCHART
No
Eyes, ears, nose, GUT
Bad Brainstem
Alcohol
This Course is about the BRAIN
Medication
Skin, joint, muscle Receptors
Segmental Reflexes
If it were nerve roots would it be the entire hand? NO
Dermatomal vs. Plexus, vs. cord
Example text
Example text
Intrinsic muscles of the hand
Ventral Horn Disease
Poximal Muscles usually Primary muscle disease
Spaticity vs. weakness
FLOWCHART
What is Cholenergic supersensitity?
Flashed a light at the throat and had him say AHHH.
Flashed a light at the nasal retina and watched both eyes
I covered one eye with my hand, then alternated between the two eyes.
I skillfully tapped his thenar prominence bilaterally
I had him follow my finger with his eyes only
I had him resist me to test his strength- hands and hips
I jerked his ankle and tapped his knee
7 Things I did
Vertigo is considered a sensory mismatch and my involve the:
Vestibular apparatus in the inner ear
The nerves growing from the brain stem
The nuclei living in the brainstem
The extraocular eye muscles and stabilization of targets on the fovea
Proprioception loss
A 50 yo Male, writer, previously treated with antipsycchotic medication, has long standing Vertigo and continued pyschiatric dysfunction.
CASE PRESENTATION- GMr
Intermediolateral Cell column S2-S4
Synapse on the rectum and genitals
Either the parasympathetics get released from inhibition, or they receive excitatory input? Which is it?
Sacral parasympatehtics
Ascending Pattern (leg is worse than arm)
Descending Pattern
Intrinsic vs. extrinsic
Sensory Dissociated – Anteriolateral system (pain and temp from opposite side, Dorsal columns ipsilaterally, light touch and vibration)
Long Tract Pattern
Doesn’t follow the
Nerve root, dermatome
Myelopathic Lesion
Marie Charcot Tooth Disease- Hi arching feet and palate
Friedricks Ataxia
Spinocerebellar Ataxia
Hereditary Neuropathy
Neuropraxia is reversible
Axonmesis or Neuromesis leads to problems like sphincter loss and are not reversible
Any and all peripheral nerve dysfunction has a central consequence.
The Take Away
The Postural Spondylogenic Reflex Syndrome:
The absence of pain does not automatically mean lack of soft-tissue findings.
It is well known that localized palpable muscle bands or systematic myotendinoses can be elicited upon careful palpation in many individuals who have no subjective pain complaints.
This situation is to be considered pathologic and correlates with the latent state of intervertebral insufficiency according to Schmorl and Junghanns (1968).
This could be explained on the basis of the tonic reflexogenic influence of the type 1 mechanoreceptors upon the motor neurons of the axial or peripheral musculature.
It has been shown that pain-inducing nociceptors have significantly higher thresholds than pain-inhibiting mechanoreceptors. This may explain the delay with which the individual may perceive his or her pain.
The Postural Spondylogenic Reflex Syndrome:
Special Senses
Type I: provide important information about joint position as they signal the angle of the articulation throughout the range of motion.
Type II: Have a low threshold and rapidly adapt to a stimulus. Detect rate of movement at the articulation.
Type III: High threshold and slowly adapting receptors. They are stimulated only at the extremes of joint movement. Structurally similar to the Golgi tendon organ of the muscular system
Type IV: Nociceptors; have a high threshold and do not adapt. These pain receptors tend to be free nerve endings.
Mechanoreceptors
Infectious disease can do the same
Neurosyphylis
Herpes leads to 20 percent increase in Alzhemiers
Can you see how peripheral nerve dysfunction has central consequences
Magnesium does it to, this is where drugs attempt to help
Or at the Neurotransmitter
Ca channel blockers
Alzhemiers (amyloid and Tau)
Dementia (Lewy bodies)
Parkisons ( A synuclein pathology)
Prions- infections disease does the same.
Corticobasilar degeneration (tau pathology)
They all are epigentic protein MUTANTS
You are what you are because of where you are in the brain. One cause. . .
Degenerative Disorders
Define Long term Depression
Define the Hebbian Process
Kinase leads to the Gene getting turned on after transcription of protein.
Then the cell can make 2nd messenger ions (N.T.)
This is called Long Term Potentiation because the cell infrastructure is in place.
This can change if I stop using ADP
Can lead to neural degeneration.
5th Messenger- the protein
Free radical damage (Nitric Oxide)
Causes interleukin cytokines to cause inflammation leading to Na imbalance= Apoptic Neuron.
This perpetuates itself
Can be perpetuated by hypoxia (Ischemic STROKE)
Ischemic stroke gives you 4 hours to get to the hospital for good emergency outcomes.
Clot busters if ischemic
Intracellular calcium is the
Disease of mitochondria? Then activation would drive the disease further- PT 3x a week, 80 adjustments a year?
Genetic Synaptic Disease
Neurotransmitter imbalance
Adrenal and renal pathology
Creatinine, albuman, GFR, U.A.
Kidney disease = Bad Brain
Electrolyte imbalance
Big picture
You can have dysfunction at any of these structures
You can have mutation of protein, the higher probability of SNPs- EPIGENTIC FALTS
Transport system can breakdown
Carrier protein transports across the cell (requires energery)
Microtubules can transported on carrier proteins as well
Cell becomes more efficent and now more synaptic success.
Then growth factors get exchanged, through retrograde Flow
This is how neural networks work as a SYMPHONY
Neurons, glial cells, oligodentracyts, astrocyte.
Glial Cells release pro and anti imflammatory cytokines. These cells are primed over time to become over sensitive.
This can lead to chronic encephalopathy
Autoimmunity, destruction of oligodendrocyte.
This is neurodegenerative disease
Can get the aceytlcholine through because intracellular architecture breaks down (cholenergic system damaged)
Alzhemers (bradykinesis without tremor)
Parkinsonian- tauopathy causes tremor, anosmia, falls, dementia,
SNP-with tremor
Neurons and glial Cells
Midline structures (reticular formation)- they fire up to activate the frontal brain
Acetylcholine and dopamine (best friends) in the b.g. (ventral mesenscephalon)
Control of eyes, collicular maps, holds head up, postural tone- this helps
develop chewing (trigeminal nucleus- that’s whys its separate, it comes first, then CN7,9,10 function become important and are bourne out of necessity.
Ocular control (horizontal and vertical optokinetics develop)
Then they start using limbs to direct food for chewing and away they go.
The more lateral columns are regulated by the brain after it takes in the midline column information
Homologus columns
Activation causes genetic transcription for a protein
Nucleus gets activate (top of the food chain)
E.R. and Golgi apparratus builds protein
Ships to transport system to different parts of the nucleus
Midochondria is power station
Stability of Cell is dependent upon neuron function
Epilepsy, autoimmune breakdown, neuron degeneration, damage from ischemia….
The Neuron
The Neuron
Neurogensis
Commissures make use of the lamina terminales.
The first to appear is the anterior commissure.
The second is the hippocampal or fornix commissure.
By the tenth week the corpus callosum develops; it begins as a small bundle through the lamina terminales and as a result of the expansion of the neopallium it extends first anteriorly and then posteriorly, arching over the thin roof of the diencephalon.
There are three other commissures: the posterior commissure, the habenular commissure, and the optic chiasma.
Immediately above the choroidal fissure, the wall of the hemisphere thickens to form the hippocampus
The lateral walls of the mylencephalon are everted (A).
Position of alar and basal plates in the mylencephalon at different stages of development (B and C).
Cells of the alar plate migrate to form the olivary nuclei (arrows).
The basal plate contains the motor nuclei and the alar plate contains the sensory relay nuclei (C).
The roof plate of the myelecephalon contains a single layer of ependymal cells covered by vascular mesenchyme together known as the tele choroidea. The tuft like invaginations are the choroid plexus.
Example of a patient with meningomyelocele (A).
Example of patient with rachischisis (B).
Third month of development (A).
End of fifth month of development (B).
Birth (C), the dura (and subarachnoid space) remains attached to the vertebral column at the coccygeal level.
A threadlike extension of the pia matter forms the filum terminale
During the fourth week of development, axons of neurons in the basal plate break through the marginal layer to form the ventral motor root (A).
Axons of neurons in the alar plate penetrate the marginal layer and ascend or descend to form association neurons.
Dorsal root ganglion neurons grow centrally and peripherally (B).
Dorsal nerve roots are collections of fibers originating from neurons in the dorsal root ganglion.
Distal processes join the ventral motor root to give rise to the spinal nerves.
Neural crest cells, in addition to developing into dorsal root neurons of the spinal and cranial sensory ganglia, they differentiate into:
sympathetic neuroblasts
Schwann cells
pigment cells
odontoblasts
meninges
mesechyme of the pharygeal arches
Neuroblast are round and apolar when they migrate to the marginal layer (A).
These then differentiate into bipolar neurons (B) with one of the processes becoming a primitive axon and the other the primitive dendrites (C).
Ventral thickening results in the formation of the basal plates (A).
These contain the ventral motor horn cells.
Dorsal thickening results in the alar plates (A).
The boundary between the basal and alar plates is the sulcus limitans (A).
Neither the dorsal or ventral midline portions of the neural tube contain neuroblasts and are known as the roof and floor plates, respectively (A).
An intermediate zone of neurons (B) contain the sympathetic portion of the ANS and are located in the thoracic and upper lumbar (L2 or L#) of the spinal cord (B).
Mouse spinal cord at a similar age to A (SG, spinal ganglion).
On the periphery of the neuroepithelial layer, differentiating neuroblasts are observed.
These form the mantle layer which gives rise to the gray matter of the spinal cord.
The outermost layer of the spinal cord is known as the marginal layer.
These contain nerve fibers emerging from the neuroblasts in the mantle layer.
Subsequent myelination results in the formation of the white matter of the spinal cord.
Sagittal view through a mouse embryo is shown.
At the 27th day, the cephalic end has 3 dilatations:
Prosencephalon (forebrain, F)
Mesencephalon (midbrain, M)
Rhombencephalon (hindbrain, H)
Two flexures are also formed:
The cervical flexure between H and the spinal cord
The cephalic flexure in the midbrain region
Formation of the neural groove, neural tube, and the neural crest (A-D).
Neural crest cells go on to develop into spinal and cranial sensory ganglia.
A mouse embryo is shown in E (similar developmental age to D).
1) Medial Somatic Motor column: dealing with the midline muscles. It stretches the length of the spinal cord and much of the brainstem;
2) Lateral Somatic Motor Column: deals with the more lateral muscles which shunt or move the extremities: hence the discontinuity of this column;
3) General Visceromotor Column: these are basically the preganglionics of the cord. They are a bit more dispersed and complicated in the brainstem. This is the most visible part of the IML
Oxidative Phosphorolation
Methylation Errors
Transcription errors
Bilipid membrane destruction
Wallarian Degeneration.
Neuron Degeneration
Did you Know?
ALL Sensory inputs Summate in the Brainstem enroute to the cortex
All Somatic sensory nerves terminate on the Nucleus Tractus Solitarius (NTS)
Facial Afferents summate on the Trigeminal nucleus
and the cortex activates itself.
Neurology of upper Cervical Subluxation and Adjustment
This Course must be about the Brain

Chiropractic directly influences genetic expression through neurophysiological activation, whether that be excitation or inhibition, peripheral and or central, neurohormonal, neuroimmunological or neuropsychological. Having a temporal effect on the organisms homeostasis either through feedback mechanisms, long term potentiation or other cortical mechanisms which can be defined.
Neurology for the Upper Cervical Diplomate
Intrinsic- Ventral horn disease, M.S., Infection, metabolic
Trunk, arm, Leg
Extrinsic- (ascending pattern)
disc spondyosis, tumor
- Pain and temp of the Leg FIRST, Arm, then Trunk
Dorsal columns of the upper extremity aslo affected but before the legs
Due to laminar distribution in long tract pathways.
Intrinsic vs Extrinsic Lesions
Transient unilateral mydiasis has been reported in basilar aneurysm- Walsh and Hoyt 1985
Above has also been reported in Arterial malformations, neuromas and aneurysms but typically comes with other signs of 3rd nerve palsy.
Ciliary ganglion damage results in Tonic pupil.

Oculosympathetic spasms observable upon vision denial.
Bilateral Mydriasis (pupilary constiction) due to medications with binocular vision in room light.
Ocular spasms without vision
Positive findings
The Pan Opthalmoscope
Intracranial and peripheral Pulse oximeters
Video electronystagmography
Posturography
Maddox rod
Convergence and Divergence test
Some equipment you should know about
CN III, IV,VI and the VHC
CN VII
CN
Clinical Homologes
Mini mental exam
Obervations of head position in relation to the thorax
Pupil position and size
eyelids
Facial tone

Interview and Observations
Brainstem and sacral divisions
Brainstem nucluei include
CN III superior colliculus andedinger westfall nucleus
CN VII Pontine tegmentum, ssn and lacrimal nuclei
CN IX Inferior Salavatory nucleus in rostral medulla
CNX Nucleus Ambiguous and DMNV
Parasympathetics
When I inhibit my IML, Parasympathetics can come to threshold
Look at urination
Bladder stretches- should urinate immediately
But the brain inhibits the sympathetics
Most of use can think a thought like, “now I shall pee”, and you can
Sympathics cause retention
Parasympathic dominace gives you urgency
IML inhibits Sacral parasympathetics
Do 4 things
1. Inhibit the Intermediolateral (IML) Cell Column
When you raise a limb you get sensory feedback from the periphery which activates the IML
Everything activates the IML accept
Descending pontomedulary system
Cortex
2. Facilitates gamma motor neuron
3. Dampens pain in dorsal horn (descending analgesic pathways
4. Inhibits vhc of flexors above t6 and extensors below t6.
Pontine and Medullary Reticular Pathways
Close to the attachment of the dentate ligaments.
Responsible for conveying pain and temperature into the neuroaxis.
Mechanical irritation and/or ischemic compromise to the spinothalamic tracts possibly explains particular cases of severe low back and leg pain being caused by an upper cervical subluxation.
The Spinothalamic Tracts
Rules from Embryology
Ventral is motor
Dorsal is Sensory
If a motor tract is in the dorsal lateral aspect of the cord it deccusated! (LCST)
Same is true for Ventral Spinocerebellar tract
Anteriolateral Ascending Systems.
Cross or not?
Alar or Basilar plate?
Alar and Basilar plates
Vascularity
Anterior Spinal artery 2/3
Posterior Spinal artery 1/3 Dorsal horns
Spinal Cord
Do you know what nerves exit at what foramen. C6 exits at C5/C6
What about L5/S1- L5
Gluteal muscles are spared in Sciatic nerve lesions
Gastroc and Glute together have to be nerve root
What about OCC/C1?
Brachial Plexus- if it’s the finger only its at the wrist.
Entrapment syndromes
Thoracic outlet Syndromes
Peripheral neurology not our clinical focus.
Plexopathies
Learn the brachial plexus presentations
Which nerve roots affect what muscle groups
Polyneuropathies
Diabetic polyneuropathy
Alcohol induced polyneuropathy
F waves will give us feedback about the proximal part of the peripheral nerve and dorsal ganglia.
Peripheral Neurology
Graded and indicate likelihood of good prognosis. (1-5)
Sunderland Classification of peripheral nerve damage.
Axon loss is sensory before motor
If Motor is affected first its usually myelin
Conduction is slow in meylin damage
NCV small- Amplitude depressions are from Axon
Axon death leads to muscle changing where acetylcholine receptors are.
Moves them to the surface to get mor activation
N.T. makes the muscle spontaneously fire
THIS IS FACICULATION- (DENERVATION Fibs and Sharps)
Peripheral Neuropathy
The nociceptive stimulation can be inhibited presynaptically when there is sufficient stimulation of the mechanoreceptors, mainly the type II receptors.
This may occur by release of endorphins: cells in the gelatinous substance of the dorsal horns.
Therefore, it would plausible to propose that these and probably other related neurophysiologic mechanisms may play at least as important a role in manual therapeutic treatment as the pure mechanical correction of one or several segmental dysfunctions.
The Postural Spondylogenic Reflex Syndrome:
The clinical symptom of pain in muscles and other soft tissues (spontaneous or elicited by palpatory pressure) has been termed the Spondylogenic Reflex Syndrome by Sutter (1974,1975).
Myotendinoses has been in observe the various systematic response to an articular/somatic dysfunction involving the individual apophyseal, occipito-atlanto-axial, and sacroiliac joints.
“Many systematic myotendinoses improve during the course of therapeutic intervention in the individual patients”.
It was therefore assumed that, in addition to other helpful physical and therapeutic procedures, the mechanical and functional correction of the spinal motion unit, according to Schmorl and Junghanns (1968), can play a significant role, if not the most crucial role in treatment.
The Postural Spondylogenic Reflex Syndrome: Clinical Correlation with Reflexes Linked to Nociceptors and Mechanoreceptors
Joint Mechanoreceptors
Muscle Spindle
Neuromuscular junction
Vision
Sound
Chemotactic
Baroreceptors
Olfactory
Nociceptors
Parcinian, meisners, Ruffini, Vestibular apparatus, Taste
Conduction- things stuck in your ear.
Senserineural- from the cochlea to the brain
Receptors - what processes can affet their function
NMDA receptor is regulating Ca,
Activated by Neurtrophic factors
Dysregulation of Ca channels
Ca degrades Phosopholipid bilayer (free radicals (phospholipase)
Causes Mitochondria to uncouple
Intracellualar calicium is the major factor for neurodegeneration
Initiates tangles and tells other NMDA channels to open
Mitochondria triggers the Ca imbalance
Read about Molecular Neurodegeneration
Apoptotic pathways
1. Neurotransmitter
2. carrier
3. Kinase
4. phosphoprotein in the Nucleus
Gene response of early genes goes on for hours to days
So when you activate this 4 Mess. pathway you strenghten pathways.
Epigentics are a 4 messenger system
With acivation comes fatigue.
Can be seen in the eyes
If it’s a horizontal diplopia without pupil or lid disfunction its CN 6
Its its in the vertical plane without pupil or lid involvement, its CN4 and resultant head tilt.
If its vertical with Pupil and lid- CN3
Happens post synaptically
Lambert Eaton syndrome is the same thing at the pre synapes, (Nerve gas does this)
Myesthina gravis- post synaptic antiodies block the cleft transmission
MSG and Aspartame should be a dietary restricted.
This can be happening in the
Limbic system- Schizophrenia
Mesencephalon- Parkinson disease
IF YOU manipulate these people you will drive the system to crash, these patients need less activation.
Oh by the way
Dentritic zone- reception
Somatic zone- Soma- integration of chemical encoding
Axon Hillock- Electrical impulse
This creates a gene response at the target nucleus to produce protein.
Cytokines and Neutransmitters (start as monoamine then Decarboxylase etc)
The golgi take it package it for the E.R. and off ya go to a secretory vessicle then
Lysosomes break it down
Neuron
Climbs the Glial Fiber
Neural Migration
Continuous growth of the cerebral hemispheres in the anterior, dorsal, and inferior directions result in formation of the frontal, temporal, and occipital lobes respectively (B).
Growth in the region over the corpus striatum slows resulting in overgrowth of the insula.
Craniopharyngiomas arise from remnants of Rathke’s pouch. They usually lie above the sella and may cause hydrocephalus and pituatary dysfunction
The hypophysis develops from fusion of Rathke’s pouch and the infundibulum (A, six week old embryo).
Development at 11 weeks (B).
At 16 weeks, the pars tuberalis and pars intermedia appear (C).
EM at high magnification that is developmentally similar to A (C) (arrow, Rathke’s pouch; arrow heads, infundibulum)
Diencephalon
The diencephalon consists of a roof plate and two alar plates but lacks a floor plate and basal plates.
A groove in the alar plates, the hypothalamic sulcus, divides the thalamus from the hypothalamus (A).
The roof plate of the diencephalon gives rise to the choroid plexus (B) and the pineal body at it’s most caudal aspect.
Mesencephalon
The basal plates consist of two groups of motor nuclei (III/IV and n. of Edinger-Westphal) (B).
The marginal layers of the basal plate enlarge and form the crus cereebri.
A transverse groove forms along the alar plates to delineate the superior and inferior colliculi.
The rhombic lips, as a result of deepening of the pontine flexure, compress and form the cerebellar plate (A).
The flocculonodular lobe appears at 20 weeks of development (B) and phylogenetically the oldest part of the cerebellum.
Early stage of mouse cerebellum at similar developmental age to A where the cerebellar primordium (C, white arrow) and choroid plexus (D, black arrow) are demonstrated.
The metencephalon has similar organization of the alar and basal groups of nuclei.
The marginal layers of the basal plates expand to accommodate fibers connecting the cerebral and cerebellar cortices with the spinal cord thus forming the pons
Cells from the alar plates migrate to form the pontine nuclei.
Mylination at the periphery via Schwann cells occurs at the beginning of the fourth month of development.
Central mylination via oligodendroglial cells occurs from the fourth month in-utero to the first postnatal year
Gliabasts are formed by epithelial cells after the production of neuroblasts ceases.
These migrate from the epithelial layer into the mantle and marginal layers and form protoplasmic and fibbrillar astrocytes.
Oligodendroglia may be produced from gliablasts and inhabit the marginal layer.
When neuroblast and gliablast formation ceases, neuroepithelial cells differentiate in ependymal cells to line the central canal of the spinal cord.
Microglia are produced from mesenchymal cells.
The lumen of the mesencephalon connects the third and fourth ventricles and is known as the aqueduct of Sylvius (arrowheads show the roof of the fourth ventricle)
The lateral ventricles and the third ventricles communicate via the intraventricular foramen of Munro.
The lumen of the spinal cord is continuous with the brain vesicles.
The cavity of the rhombencephalon is the fourth ventricle.
The cavity of the diencephalon is the third ventricle.
The cavities of the cerebral hemispheres of the telencephalon are the lateral ventricles.
At 5 weeks old, the prosencephalon consists of two parts:
Telencephalon (T)
Diencephalon (D) noted by the outgrowth of the optic vesicles (o).
A deep furrow, the rhombencephalic isthmus, separates the mesencephalon from the rhombencephalon (arrow).
The rhombencephalon also consists of two parts:
Metencephalon (Mt) which later forms the pons and cerebelum
Myelencephalon (My)
The metencephalon and the myelencephalon are divided by the pontine flexure.
Fusion of the neural tube begins in the cervical region and proceeds in cephalic and caudal directions (A).
Fusion is temporarily delayed at the poles creating a cranial and caudal neuropore (B). These close at the 25th and 27th day, respectively.
A mouse embryo is shown in C (similar developmental age to A).
Early development
CNS begins in 3rd week with thickening of ectoderm to form the neural plate (A, dorsal view) rostral to the primitive pit.
The lateral edges then elevate to form the neural groove (B).
A mouse embryo is shown in C (similar developmental age).
Helps us understand the nervous system
Homologues
Longitudinal 3 dimensional understanding of N.S.
Not cross sectional.
Chiropractors activate suprasegmental structures via receptor systems or environmental change of the spinal cord or brainstem
Which leads to changes in regulation of these same homologues columns, which have affects segmentally
And of course the neuron drives this process, that bring us understanding the process of Synaptic Transmission of the Neuron
Why Embryology is important
Descending Pattern
Not long track signs- grey matter lesions!
Loss of pain and temperature because these pathways cross ventral to the central canal
Shawl like distribution due to more lateral aspects of the body are represented in the midline
Intrinsic lesions like a Syrinx
CN III
CN V
CN IIX
CN IX and X














Accomodation/Pupillary to light
Corneal Reflex
Vestibuloocular
Gag
Reflexogenic systems can give real time feedback about the health of a pool of neurons.
Typically the first pass is indicative of the resting state of the system.
(Just like in cerebellar tests of acurracy )
Brain Stem Reflexes
Pyramidal
Extra Pyramidal (non volitional)
Renshaw cell- actively inhibits the VHC to keep it healthy.
Motor Pathways
The spinocerebellar tracts lie along the lateral edge of the spinal cord (the most probable site of maximal mechanical irritation by the dentate ligaments).
Proprioceptive tracts, which regulates muscle tone and joint position sense.
Irritation of these tracts could lead to muscle tone imbalance of the pelvic girdle resulting in a functional short leg.
The Spinocerebellar tracts
Neuropraxia= neural conduction signal block
Axontmesis- transection of the axon
Compression or trauma
Neurotmesis- Perineum severed.
Permancy of symptoms
Denervation, muscle fibrosis
Types of peripheral nerve damage
NMJ
Entrapment
Metabolic
Sensory before motor
Epineurium with bundles of nerves covered with perineurium and endoneurium
Epineurium is protective
Perineurium protects against stretch
Vasculature is also present and is suseptiple to compression (leg fall asleep)
Peripheral Nerve Damage
MRI, CSF
Symptoms are varied
May have afferent pupillary defect
Multiple Sclerosis
Sodium rushes in
Potasium moves out
Net charge goes down
Lead to hyperpolarization and refraction
This is the thing, Na and Potasium need help getting back
A pump is required
If the top dog is tired, he may not help get ya back
This leads to a swollen cell
Resting membrane potential gets closer to threshold
Spontaneous activity.
ADP and P can’t get used to make ATP
P break down the membrane and open NMDA recpetors
NMDA receptor gets activated by peripheral system- This is what reciprorcally causes the gene respone
This lets calcium into the cell and attacks the nucleus when no activation occurs.
This causes protein degradation
Mitochondrial damage
Excytotoxic cells (glutamate mediated)Neurodegenerative disease.
Action potential
Telencephalon
Consists of two lateral outpocketings, the cerebral hemispheres, and a medial portion, the lamina terminales.
By the second month, the basal part of the hemispheres bulges into the lumen of the lateral ventricles to form the corpus striatum. It is divided into the caudate nucleus and the lentiform nucleus by the passage of the internal capsule fibers (B).
The choroid plexus forms at the medial attachment of the hemispheres to the roof of the diencephalon (B).
The cerebellar plate contains neuroepithelium, marginal and mantle layers (1A).
The neuroepithelium migrate to the surface of the cerebellum to form the external granular layer (1B) which gives rise to the granule cells (2A).
Basket and stellate cells derive from proliferating cells in the cerebellar white matter
The figure shows the brain vesicles in an 8 week old embryo with the roof of the rhombencephalon removed.
Rhombencephalon
Myelenchephalon gives rise to the medulla oblongata.
All cranial nerves arise except I-III arise from the rhombencephalon
Spina bifida occulta occurs in 10% of healthy people and is situated from L4 to S1 (A).
Spina bifida cystica is when meninges (B) and/or neural tissue protrudes (C) through the bifid defect. These are usually not associated with mental retardation. Arnold-Chiari malformation is virtually always present.
Occasionally the neural folds do not elevate but remain as flattened masses (D and E). Associated hydrocephalus due to cord tethering and pull of cerebellum into foramen magnum.
Neural tube defects
Defects of the spinal cord resulting from abnormal closure occur in the third and fourth weeks of development.
Spina bifida is the splitting of the vertebral arches.
The incidence of severe neural tube defects is 1/1000 births.
Spinal cord
The wall of the closed neural tube consist of neuroepithelial cells.
These are arranged in psuedostratified epithelium and extend over the full width of the wall.
Dividing neuroepithelial cells are located at the lumen side of the tube.
Median
axillary
Musculocutane
radial
Ulnar
5
6
7
8
1
Tricks to draw Brachial Plexus 3333
FLOWCHART
No
Methylation errors
Bilipid membrane breakdown (Omega 3 F.A.)
Neuron Dysfunction
Medication,
Oxidative phosphoralation
If it were nerve roots would it be the entire hand? NO
Dermatomal vs. Plexus, vs. cord
Example text
Example text
Intrinsic muscles of the hand
Ventral Horn Disease
Poximal Muscles usually Primary muscle disease
Spaticity vs. weakness
FLOWCHART
Neurons grow on Glial Ladders, they compete, connect and activate through synaptogensis.
Hard wiring is driven by functional activation in the fetus
FLOWCHART
Migration
differentiation
Neurophysiological consiquence
Physical distress to tissues
Neurogensis
Structural subluxation
W/o atrophy, weakens with activity
Peripheral Nerve
Neuro
muscle junction
Primary Motor disease
FLOWCHART
VHC
Yes
Weakness, proximal vs distal, Faciculations, atrophy, Sensory?
Proximal Muscle weakness
Distal muscle weakness
Neurons grow on Glial Ladders, they compete, connect and activate through synaptogensis.
Stem Cell
Neurogensis
Migration
differentiation
Neurophysiological consiquence
Physical distress to tissues
Selection, competition then dentrictic
Neurogensis
Structural subluxation
Example text
This is an example text
Example text
This is an example text
Example text
This is an example text
Sleep Apnea, Palatal weakness,
Example text
This is an example text
Your Gut dysfunction will destroy the brain
Repiratory asdiosis
Thyroid Disease
Dysglycemia
Anemia
Metabolic conditions create irritability
No
Understand what can affect neurological function
Loose inhition of Embryologic flexors in axial musculature
BRAIN
No
No
No
Bad Cognitive
Loose inhition of Autonomic/gut dysfunction
Pain isnt inhibited
FLOWCHART
No
Eyes, ears, nose, GUT
Bad Brainstem
Alcohol
This Course is about the BRAIN
Medication
Skin, joint, muscle Receptors
Segmental Reflexes
If it were nerve roots would it be the entire hand? NO
Dermatomal vs. Plexus, vs. cord
Example text
Example text
Intrinsic muscles of the hand
Ventral Horn Disease
Poximal Muscles usually Primary muscle disease
Spaticity vs. weakness
FLOWCHART
Think like a neurologist X.X.
Learn how the nervous system is organized
Be able to think through a lesion to understand its pathomechanics origins (when neurogenic in nature)
Become either aquainted or requainted with current concepts of neurological disorders.
Clinical Practice
CASE of 74yo
One of your right handed 74 yo female patients with known hyperlipidemia awakes with Left arm heaviness
1
Primary Diagnostic Process?
Observations
History Taking
Signs and Symptoms
Phenomenology is a useful methodology for describing and ordering experience. As such, phenomenology can be specifically applied to the first person experience of il
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