Neuro Flashcards
LL Neuro Schpiel
Today I examined ____ lower limb.
Pertinent findings were weakness in XXX with tone/reflexes/co-ordination/sensory findings of ____.
These findings are in keeping with an upper/lower/mixed motor neuron pattern consistent with a lesion at the XXXX.
My differentials are ….
Schpiel (Gait)
Today I was asked to examine ____ gait, which was ____.
Given these findings I went on to examine lower limb neuro, co-ordination/cerebellar/Parkinson’s.
My findings were ___ consistent with ____ and my differentials are _____.
-
Predominant sensory peripheral neuropathy causes
- Diabetes
- ETOH
- Hypothyroidism
- Uraemia
- Sarcoidosis
- Paraneoplastic
- B12 deficiency
- Infections, e.g., leprosy, HIV, Lyme disease
- Amyloidosis
- Drugs (isoniazid, metronidazole, hydralazine, disulfiram, chloroquine, pyridoxine, colchicine, flecanide).
Predominant motor peripheral neuropathy causes
- CIPD/GBS
- Drugs (Dapsone)
- Porphyria
- Lead
- Diptheria
Pes Cavus (inherited neuropathy) causes
- CMT
- Friedrich ataxia
- Muscular dystrophy
- Cerebral palsy
- Spinal cord tumour
- Poliomyelitis
- Syringomyelia
- HSP
Axonal loss signs
(Diabetes, ETOH, malignancy)
- Distal reflex loss
- Distal proprioception/vibration loss
Demyelinating loss signs
(HIV, drugs, MS)
- global areflexia
- decreased proprioception/vibration
- preserved pin-prick
Proximal limb weakness causes
Proximal myopathy:
- steroids, ETOH, statins
- diabetes, diabetic amyotrophy
- thyrotoxicosis
# IBM (quads) # Polymyositis/dermatomyositis # Mitochondrial myopathies # Hereditary causes - muscular dystrophies, fascioscapulohumeral dystrophy
Distal myopathy causes
- Myotonic dystrophy - facial and distal limb weakness, myotonia
- IBM (distal in UL)
Lower limb weakness differentials
# Mix of UMN & LMN with no sensory findings: - MND, cerebral palsy, lacunar infarct
UMN in upper and lower limbs, bilaterally:
- High cervical stenosis
- MS
- Arnold chiari malformation
LMN lesion in UL and UMN lesion in LL
- Syringomyelia
- Cervical lesions
Sensori-motor peripheral neuropathies:
- Inherited: CMT
- Acquired: Diabetes, CIDP
Neuromuscular disease:
- Myasthenia
- Lambert Eaton
Foot drop causes
Weak tibialis anterior
Common peroneal lesion - loss of eversion, sensory loss over lateral calf/dorsum of foot
L4/L5 root weakness - loss of eversion and inversion, expect dermatome sensory findings, may have hip abduction weakness
Bilateral peripheral neuropathy - all movements weak in glove/stocking sensory loss and areflexia.
UMN pattern:
- bilateral spastic paraparesis - spinal cord lesion, bilateral stroke, MND
- One leg weak - cortical infarct/lesion, Brown-Sequard
- Hemiparesis - Upper and lower limb weakness same side - ? stroke
Sciatic nerve lesions - loss of eversion/inversion and ankle jerk.
Anterior horn cell disease - polio
Other neuro spiel
- It is best to mention abnormalities as patterns rather than coming up with a diagnosis first up, e.g.,:
- UMN vs LMN or a combination
- Cerebellar dysfunction +/- other signs
- Peripheral neuropathy (sensory/motor)
You can then mention a list of possible diagnoses.
Neuro Cases
- Polyneuropathy - others (pure motor, sensorimotor - 21%
- Muscular dystrophy - myotonic - 14%
- CN lesions including pituitary tumours - 13%
- Multiple Sclerosis - 12%
- Myopathy/myositis - 12%
- Polyneuropathy - CMT - 7%
- MND - 7%
- Parkinson’s disease/PSP/Huntington’s
- Stroke - 7%
- Polyneuropathy - Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
Ability to stand on toes?
S1
Ability to stand on heels?
L4,5 –> foot drop
Romberg test
Steady with eyes open, unsteady with eyes closed:
- posterior column
- peripheral neuropathy
- vestibular function
Unsteady with eyes open & closed:
- cerebellar
*Unlikely to be related to cerebellar function in exam
Diplegic/paraparetic gait causes (5):
- SC lesion
- Cerebral palsy
- Bilateral strokes
- HSP
- MS
CP Lesion (foot drop)
CP CAN invert whereas L4/L5 or Sciatic lesions unable to invert.
CP, L4-5 or sciatic lesions CAN’T evert.
Ankle jerk preserved
Unilateral high stepping gait (unilateral foot drop) causes:
Distal weakness:
- L5 lesion
- CPN lesion
- Sciatic neuropathy - patient can walk on toes but not heel of affected side
Bilateral high stepping gait (bilateral foot drop) causes:
- Lumbosacral polyradiculopathy
- MND
- Distal polyneuropathy e.g., CMT (patient can’t walk on heels or toes), CIDP
- MD
High stepping gait of sensory neuropathy (sensory ataxic gait) causes:
Maybe wide-based, clumsy, slapping down of feet + Romberg’s:
- Peripheral sensory neuropathy
- Syphilis
- Subacute combined degeneration of the spinal cord
UL/LL Neuro *Don’t forget:
1) Scars, back, neck
2) Catheters
3) Peri-anal sensation, anal tone
Gerstmann’s syndrome (Dominant) - 4
1) Agraphia
2) Acalculia
3) Finger agnosia
4) Left-Right Confusion
Subcortical lesion:
- Internal capsule
- Basal Ganglia (Globus pallidus & Putamen)
- Thalamus
- Absent cortical signs
- Face, arm & leg equally affected
- Unusual movements (basal ganglia)
- Dense sensory loss (thalamus), maybe associated with hemiplegia
Brainstem lesion (5)
- Crossed hemiplegia, cranial nerve or cerebellar signs on side of brainstem affected opposite to hemiplegia
- Nystagmus horizontal, vertical
- INO (Internuclear ophthalmoplegia)
- Gaze palsy looking to side of lesion (pontine gaze centre controls gaze towards itself)
- Sensory findings: crossed sensory loss, 5th nerve (pain & temp) opposite to body sensory loss (spinothalamic)
Cortical signs (4)
- Aphasia
- visuospatial neglect
- gaze deviation
- visual field defects
*always absent in subcortical/lacunar strokes
Lacunar syndrome (5)
- Pure motor stroke/hemiparesis (most common lacunar syndrome: 33–50%)
- Ataxic hemiparesis (second most frequent lacunar syndrome)
- Dysarthria/clumsy hand (sometimes considered a variant of ataxic hemiparesis, but usually still is classified as a separate lacunar syndrome)
- Pure sensory stroke
- Mixed sensorimotor stroke
SC Lesion
- usually bilateral
- sparing of face, cranial nerves (rarely 5th nerve long tract affected)
- horner’s high spinal lesion, sympathetic chain down to T1, T2
- sensory level
- bladder, bowel dysfunction
- if unilateral look for Brown Sequard- hemitransection of the SC:
- ipsilateral spastic hemiparesis, loss of vibration & proprioception
- contralateral loss of temperature & pin-prick
CN 2 (4)
Optic Nerve:
1) Acuity (done first)
2) Fields
3) Pupil response
4) Fundi
Bi-temporal heminopsia (tunnel vision) causes:
1) Pituitary adenoma
2) Craniopharyngioma
3) Neoplastic - meningioma
4) Vascular origin is an aneurysm of the anterior communicating artery
CN 3 Palsy
Oculomotor
1) Ptosis
2) Inferolateral displacement of the ipsilateral eye (SR, IR. MR, IO)
3) Pupil
*PCOM Aneurysm - CTA
- MRI - stroke (ischemia), tumour, demyelination, GCA, infectious
Argyll Robinson Pupil
- Accommodates but does not react.
- bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not constrict when exposed to light).
- highly specific sign of neurosyphilis
RAPD (MG)
- observed during the swinging-flashlight test where upon the patient’s pupils dilate when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.
- most common cause is a lesion of the optic nerve (between the retina and the optic chiasm) due to glaucoma, or severe retinal disease, or due to multiple sclerosis.
Common causes of CN palsies (4)
1) Diabetes
2) Aneurysm
3) A vascular event
4) Mass lesion
Complex ophthalmoplegia (4)
1) Graves
2) MG
3) Mitochondrial myopathies - Chronic progressive external ophthalmoplegia
4) Occulopharyngeal l dystrophy
Stroke facial nerve
- spares forehead
- paralysis of contralateral lower face
Pseudobulbar palsy causes:
- Bilateral UMN Lesion
- Causes: MND, MS, multiple strokes, trauma, BS tumour
Bulbar palsy causes:
- Bilateral LMN Lesion
- Causes: MND, MG, GBS, Infarcts in medulla, Polio, Arnold Chiari malformation
Dysphasia types (4)
- Receptive - can’t comprehend what you’re saying and have a problem with repeating what you’re saying: Wernicke’s area - posterior section of the superior temporal gyrus, dominant cerebral hemisphere
- Expressive (motor aphasia): Brocca’s area - inferior frontal gyrus of the dominant hemisphere
- Nominal dysphasia: can’t reliably be localised
- Conductive: arcuate fascicles - deep white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. *can’t repeat statements or name objects but can follow commands.
Dysarthria (3)
- Cerebellar (scanning speech: slow, jerky, slurred and often explosive, broken up into syllables
- UMN
- pyramidal (spastic) dysarthria: slow, laboured, patient trying to squeeze words out
- extrapyramidal e.g., PD: motonous, bradykinesia, muscular rigidity
- apraxic speech: pre-frontal motor dysfunction, difficulty constructing speech
- LMN
- nasal, flaccid (MG, MND with LMN signs, bulbar palsies)
- facial muscle weakness –> slurred speech
Posterior Column Lesions causes
1) Sub-acute combined degeneration of the cord - B12 deficiency - diet, malabsorption
2) Tabes dorsalis - syphilis
3) Friedrich’s taxia
4) Spinocerebellar ataxia
5) Paraneoplastic DRG-opathies
Syringomyelia
- ko’s the Spinothalamic tract
- spares the DCML
PD extra tests:
1) measure postural BP (autonomic dysfunction)
2) assess cognitive function (MMSE)
3) assess handwriting (micrographia)
Parkinsonism
1) BK with at least one of:
- tremor
- rigidity
- postural instability
PD
- Neurodegenerative disease caused by disruption of dopminergic neurotransmission in the basal ganglia. Loss of dopaminergic neurons in the substantia nigra.
CMT description
- Symmetrical distal motor and sensory neuropathy.
- Hyporeflexia