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Grand rounds - precipitous loss of neurologic function

Highlights the diagnostic approach to a patient with precipitous loss of neurologic function.

Peter Williams

on 29 May 2013

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Transcript of Grand rounds - precipitous loss of neurologic function

No fasciculations seen (MND - )
Tone increased - clasp knife
Power: upper flexors 5/5, upper extensors 4/5, left hand 3/5
Proprioception normal
Brisk reflexes (MND, MS + )
Vibration normal
Sensation normal (MS - )
Babinski: left up going, right equivocal Precipitous loss of function over month
SOBOE, walking (MND + )
Cold legs
Decreasing power bilaterally (L worse) (MND +, MS +)
Denies tremor (PD - )
If sneezes - falls over due to force
Denies sensation disturbance (MS - )
Slow movements: walking, fine motor, e.g. buttoning (PD +)
L sided 'twitching' ?fasciculations (MND + )
Denies swallowing difficulty
Denies recent illness Instability:
Iatrogenic (i.e. polypharmacy):
Intellectual impairment: Peter Williams, med 4000, week 10, 10/04/2011 Social history Never smoked
Drinks rarely
Denied illicit drug use
Work: former interstate truck driver
ADLs: previously coping, now struggles to wash, feed and clothe self.
Vaccinations: remembers having as a child
Home: previously living at home with wife, 5 children who are supportive (Note: other staff got the impression of an unsupportive, dysfunctional environment) Falls - high risk Mood: "short tempered"
"why me?"
~ 10/10
Denied low mood
Denied lability of mood (MS,MND - ) Past medical history Essentially none!
No medications (prior to admission)
Allergies: NKA
Denies ever having any medical conditions including stroke, hypercholesterolaemia, hypertension, PVD history NO - doesn't have PVD Hair loss
PVD risk factors: male sex, age Examination Skin intact - no ulcers
Good peripheral pulses
Good temperature
Hair loss noted starting at mid calf
Swift capillary refill time L worse than R
Denies claudication
Rest does not make it better
No ulcers
No swelling
Bilateral (PVD usually unilateral initially) YES - has PVD PVD examination PVD conclusion No PVD MMSE Pseudobulbar affect Labile mood, in particular unprovoked crying or laughing episodes
May occur in any brain insult, i.e. MND, MS, CVA, PD, dementia ~10 falls in the past two months.
Last fall one week previously: climbing steep stairs, lost balance, no loss of consciousness or significant injury.
Denies problems with hearing, vision or proprioception/sensation
Denies postural hypotension (may not be able to get up fast enough though!) History Examination Differentials HPI - timeline November 2010 December 2010 Jan 2011 Feb 2011 March 2011 April 2011 Presented to GP
Slurred speech
Neurologist consult arragned Saw neurologist at hospital
Preliminary diagnosis made
Referal for specialist neurologist consultation at Bethlehem Admitted to Bethlehem Family history No known history of neurologic disease
5 kids, all living at home, no health issues, ages 22 – 9. Five I's of geriatrics previously getting about independently, albeit slowly, now believes he will need a 4WF, willing to use one. not relevant - on no medications previously continent of both urine and faeces
Increasing urinary frequency: prior to November 2010, 4/day, now 12/day (PD + ) Leading cause of death and disability in patients > 65 Denies changes in memory or concentration
MMSE covered in examination Investigations Diagnosis No micrographia (PD - ) 29/30 - essentially normal No spatial neglect No constructional apraxia Apraxia = inability to perform sequence of activity NOT due to motor or sensory deficit
Constructional apraxia is inability to copy and 'construct' 2 or 3D forms
Deficiency might point to parietal or frontal lesion
Usually only if lesion is right-sided (same reason as neglect) Neglect = 'error' in processing imagery, NOT due sensory deficit
Blank side of clock may suggest lesion in contralateral side
Usually right parietal lobe as left lobe processes both fields (as left lobe is usually dominant in right handed persons). Parkinson's disease Multiple sclerosis Huntingon's disease Motor neuron disease Guillian-Barre syndrome Spinal cord compression Drugs Denies ever having SOB prior to Nov 2010
Now SOB on ADLs, i.e. getting worse, fast
Not worse at night, needs no extra pillows
Never wakes breathless Mr F was alert, oriented, SOOB and cooperative The basics Reduced facial expression ?masked-facies (PD + )
Bilateral vesicular breath sounds of normal intensity ?reduced expansion
Abdomen soft and non-tender, bowel sounds present
Peripheries warm and with swift capillary refill Cranial nerves Essentially NAD except...
Jaw jerk brisk
Good soft palate rise (MND - )
Strong cough (MND -)
Positive glabellar tap (PD +)
SCM and trapezius: NAD
No tongue wasting, weakness or fasciculation (MND - )
Slow, dysarthric speech (MND, MS +) Cerebellar Drift NAD
Dysdiadochokinesis: left worse than right
No nystagmus
Speech: slow, slurred, dysarthric
Tone: increased (i.e. not hypotonia)
Past pointing yes, but no intention tremor
Coordination: poor
Gait: wide base, tendancy to festination (PD + ) Peripheral Spinothalamic Dorsal/posterior column-medial lemniscus Two basic ascending/sensory pathways Path: from spinal cord (spino) to thalamus (thalamic)
Actually two pathways: anterior (crude and light touch) and lateral (pain and temp)
Senses: pain, temperature (also light and crude touch in the anterior - dorsal column also carries touch)
Decussates: spinal cord Spinal cord: Like a bra
Remembering anterior horns...
Motor, bits that move at bottom
Sensory is the other spasticity/
clasp knife rigidity "lead pipe" hypertonia extrapyramidal
static resistance
May be interrupted by tremor, giving intermittent resistance, i.e. 'cogwheel' rigidity
Out patient had NO 'cogwheel rigidity', PD - pyramidal
resistance mostly to extention (upper), flexion (lower), i.e. antigravity muscles
resistance followed by 'giving way' near end of movement Path: from spinal cord to thalamus
Senses: vibration, proprioception, light touch
Light touch is also transmitted in the anterior spinothalamic pathway (decussates at spinal cord) and is therefore not as sensitive a test for the posterior column-medial lemniscus pathway.
Sometimes called cuneate and gracilis pathway.
C1 – T6 = cuneate, > T6 = gracilis.
Decussation: medulla. Motor nerve conduction studies - NAD (MND - )
Bloods - NAD
Imaging - NAD
Respiratory - borderline restrictive pattern (MND +) MR brain
Essentially NAD
No demyelination (MS -) No results suggestive of infection Primitive reflexes come back in
Non-pathologic: old age or pathologic frontal lesion...
Dementia, space occupying, PD, MND
Isolated reflex may not be pathologic Four main primitive reflexes to test
Glabellar (PD)
Mouth: Rooting, sucking and pout
Grasp What's the problem?
Extrapyramidal disease affecting...
Dopamine-producing cell death in the substantia nigra
Males > females (slight), older age > 50 Clinical features TRAP mnemonic
Tremor 'pill rolling'
Asymetric onset/akinesia - really bradykinesia
Postural instability What's the problem?
Chronic inflammatory CNS disorder
Autoimmune attack of myelin sheaths
Demyelinated plaques in distributed in space and time
Females > males, usually 20 - 45
Incidence rises with distance from equator - vitamin D?
Our patient - primary progressive? Clinical features
Mostly UMN Optic nerve
Monocular Optic neuritis (~60% will be diagnosed with MS)
Monocular vision loss, "frosted glass"
Relative afferenet pupillary defect Brainstem, cerebellar, neuro
Unsteady gait
Impaired swallowing
Tremor (intention)
UMN signs
Emotional lability Cervical nerve roots
Sensory disturbances (posterior columns and spinothalamic)
45% of sufferers present with sensory symptoms
weakness More clinical features
Increased tone, 'lead pipe'
Impaired fine motor skills
Autonomic dysfunction (e.g. urinary frequency)
Difficulty initiating movement
Festinating, shuffling gait
Mask-like facies
Glabellar tap +ve
Speech: soft, monotone What's the problem?
Progessive neurodegenerative disease
Motor neurons (both UMN and LMN) degeneration
Comes in three clinical onsets: respiratory, bulbar or limbs
Generally "mixed picture" of UMN and LMN
Is really a set of three related diseases: amyotrophic lateral sclerosis (UMN and LMN), primary lateral sclerosis ('pure' UMN) and progressive muscular atrophy ('pure' LMN) Clinical features
Weakness, limbs, SOB - diaphragm weakness
LMN: Fasciculations
UMN: hypertonia, hyperreflexia
Generally NO sensory deficits
Labile affect
Bulbar deficits: dysarthria, dysphagia Neuro Grand Rounds Diagnostic approach to precipitous loss of neurologic function PC - slurred speech, NOT due to EtOH Mr F, 57 year old gentleman presented to his GP in November 2010 with slurred speech.
Since then increasing weakness and worsening speech
March 2011, seen by Bethlehem neurologist The case Upper veruses lower motor signs Fasciculations no yes
Wasting no yes
Hyperreflexia yes no
Hypertonia yes no
Clonus yes no
Babinski yes no
Power 'pyramidal weakness' reduced UMN LMN Approach NOT giving the diagnosis first
We'll look at a differential list
Then try and figure it out
Neuro diagnosis not always final, hence circular arrows
Videos of real signs used - with permission - in private YouTube video Background Other cases of neglect: Working diagnosis: most likely to be MND of bulbar onset
Despite is relatively spared swallow, cough, etc
Mostly an entirely UMN.
Minor extrapyramidal component but NOT PD.
Cerebellar signs - probably not cerebellar as don't fit with bigger picture and some are 'not localising', e.g. his 'unilateral dysdiadochokinesis' means it's probably a lesion elsewhere
Unusual that he had negative nerve conduction studies: these are usually very helpful in diagnosis and his negative result is why he's had second and third neurologic opinions. Terminology Bulbar = of the medulla (looks like a swelling or 'bulb' atop spinal cord), where nuclei of CN 9 - 12 are (swallowing, cough, etc)
Psuedobulbar palsy = UMN
Bulbar palsy = LMN Neuro temporal sieve Seconds: vascular, e.g. CVA
Minutes: metabolic, e.g. DKA
Hours: infective, bacterial
Days: infective, viral
Weeks: inflammatory, e.g. MS
Months: neoplasms, e.g. metastatic lesion
Years: degenerative, e.g. dementia, PD Where to from here? PEG tube now?
Non-invasive ventillation (CO2)?
Advanced care directives
Appropriate care, at home now Two up (sensory) and two down (motor)
All named based on where they go,
e.g. spinothalamic, from spine to thalamus, therefore, it is an ascending or sensory pathway
e.g. corticospinal, from cortex to spinal cord, therefore, it is a descending or motor pathway Pathways Sensory Motor Two basic descending/motor pathways...
Corticospinal/Pyramid = voluntary movement
Extrapyramidal = involuntary movement Spinal cord Two basic descending/motor pathways Corticospinal/Pyramidal Path: from cortex to spinal cord
Voluntary motor control
Goes through bits of spinal cord that look like pyramids
Two bits: anterior (only 10%, decussates at spinal cord) and lateral (the big daddy, 90%)
Decussation: medulla (lateral). Catch-all group, lots of pathways in this
Everything BUT the pyramidal tract
Function: autonomic motor or involuntary motor
e.g. facial expression, this is why you get masked facies in Parkinson's disease
e.g. also why you get tremor, etc Extrapyramidal Dorsal/posterior horns (sensory) Ventral/anterior horns (motor) bra model Case reminder...
Mr F, 57 year old gentleman presented to his GP in November 2010 with slurred speech.
Since then increasing weakness and worsening speech
March 2011, seen by Bethlehem neurologist Normal pressure hydrocephalus ***Please note: videos will not play (unless Pete logs you in) as they're currently set to 'private'***
Full transcript