Neurology-localisation

Common
Neurology
Cases

Bilateral lower limb weakness

The key features to discern are:
Upper and lower motor neurone pattern of
weakness
Is sensation normal?
What is the pattern of sensory deficits?

Proximal weaknessdistinguishing features

Myasthenia gravis- fatiguability, bulbar,
ocular and respiratory involvement
MND-fasciculations and wasting; bulbar,
and respiratory involvement; ocular
sparing. Mixture of UMN and LMN signs

Myopathy-additional points
Causes:
Acquired; inflammatory (PM, DM), endocrine
(hyperthyroidism, Cushings syndrome), toxic (statins,
fibrates, colchicine, AZT, chloroquine),
Inherited: dystrophy (Myo Dystrophy, FSH, Beckers,
LGMD, rare-distal myopathy)
Investigations:
CK, EMG and muscle biopsy.

Peripheral Neuropathyadditional points

Causes
Diffuse polyneuropathy: DM, CRF, B12 def,
hypothyroidism, GBS/CIDP, Sjogrens syndrome,
CMT, Drugs (cisplatin, vincristine, taxol (S>M),
thalidomide, pyridoxine, ddI, ddC, d4T,, INH (S>M), ,
chloroquine ), HIV, toxins (alcohol, lead and nhexane), Paraneoplastic.

Multiple mononeuropathy: Vasculitic neuropathy,

Leprosy, multiple entrapment neuropathy, MMN
(Those in bright red font cause sensory neuropathy)
Investigations: NCS, EMG, spinal tap

Wasted hands

MMN:multifocalmotorneuropathy

MMN:multifocalmotorneuropathy

MMN:multifocalmotorneuropathy

MMN:multifocalmotorneuropathy

MMN:multifocalmotorneuropathy

One wasted hand-key pointers

Wasted thenar:
consider distal median Tinels, split IV finger numbness -CTS
Benedictan sign and loss of O sign- proximal median

Wasted hypothenar-intrinsics:
Consider ulnar- split IV finger numbness, Froments sign.
Usually compression is at elbow, but know how to differentiate wrist
vs elbow ulnar palsy

All muscles wasted-segmental vs combined median and ulnar

nerve palsy.

Bilateral wasted hand

Bilateral thenar wasting: Consider bilateral median

-CTS
Bilateral hypothenar-intrinsic wasting: Bilateral ulnarusually compression at elbow, often in the
background of polyneuropathy.

Both muscle groups wasted-see overleaf

Other mononeuropathies

Cranial neuropathy

ptosis

Difficulty with speech

Speaking difficulty
Dys/a phonia
Dys/an arthria
Dys/a phasia

Dys/aphonia

Local: vocal cords/larynx

Neuromuscular junction:MG
Nerves: IX-X, recurrent laryngeal.
Think- base of skull (NPC)/, jugular foramen
(mass lesions), neck-thorax (recurrent laryngeal
nerve) and GBS/MFS
Brainstem: medulla

Dysarthria
Flaccid
Neuromuscular junction :MG
Nerve:IX-X--think base of skull,jugular foramen
-neck (mass lesions); GBS/MFS
Brainstem: medulla
Spastic
Bilateral subcortical/cortical- pseudobulbar palsy
Cerebellar
Extrapyramidal: PD

Dysphasia
Is naming affected?
2. Assess fluency: speech cadence-rhythm,
grammar and frustration from inability to
express.
3. Comprehension- test 1-2-3 step commands
4. Confirm if the associated signs are
consistent with dysphasia localization
Optional step:
Repetition
1.

Type

naming

fluency

comprehension

Other clues

repetition

Global

poor

poor

poor

Drowsy, eye deviation,

dense BF weakness

poor

Brocas

poor

poor

good

Dysarthria, dysphagia
brachiofacial weakness

poor

Wernickes

poor

good

poor

No weakness. VF
deficit

poor

Conduction
(not important)

poor

Not bad

good

VF deficit.
Parietal lobe signs +/-

Fluency when repeating

is >> worse than during
spontaneous speech

Transcortical Broca

poor

poor

good

Signs of subcortical
stroke

good

Transcortical
Wernickes

poor

good

poor

Signs of subcortical
stroke

good

Poor vision

Bilateral poor visionnon-refractory causes

Bilateral (sequential) optic neuritis (MS)

Bilateral (sequential) AION (arteritic usually but nonarteritic can be sequential too)
Untreated raised ICP (pseudotumour cerebri)
Retinitis pigmentosa, chorioretinitis
Bilateral occipital lobe disease: PRES, posterior
circulation disease (normal pupillary reaction)

Gait analysis-important points

Do not over-commit.
Keep a second or third choice up your
sleeve
Further examination is necessary

Gait-unsteady, ataxic
Cerebellar
Sensory ataxia-either dorsal column or
sensory neuronopathy

Romberg's sign may be useful

Beware of mimic: severe spasticity (e.g.

from Cx myelopathy) or gait apraxia

Gait-extrapyramidal

Parkinsonism

Beware of gait apraxia

Gait-spastic
Hemi or bilateral
Beware of mimic from apraxic gait

Gait- apraxic gait

Ignition failure
Small short, magnetic steps with poor ground clearance
Turning in numbers

Causes: NPH, Binswangers disease, Frontal lobe

dysquilibrium
Beware of ataxic and spastic gait mimicking apraxia

Gait patterns- High stepping

Uni/bilateral foot drop
Beware not all patients with foot drops have high
steppage!
Severe sensory loss
Causes:
Severe non-length dependent sensory neuropathy
or sensory neuronopathy. Reflexes should be
significantly reduced.
Dorsal column dysfunction including that from
high cervical myelopathy

Gait- Waddling

Proximal myopathy

Beware hip pathology

Hemiplegia
Basic limb examination
BS signs
Right hemisphere: VF, sensory and visual
neglect, constructional apraxia
Left hemisphere: Language, VF, sensory
and visual neglect
Causes; stroke, pri/sec. tumours, CVT

Visual field- patterns..know

causes
Bitemporal
Homonymous-hemi/
quadrantanopia
Central scotoma
Altitudinal

Cerebellar- exam. steps

Eyes-nystagmus, poor pursuit, saccadic
dysmetria
Speech-staccato
Upper limbs-dysmetria, dysdiadokinesia
Lower Limbs-abnormal heel shin test
Gait-ataxic gait

Cerebellar-causes

Congenital: SCA, AChiari malformation

Metabolic/endocrine: Hypothyroidism
Inflammatory/Infectious: MS/ADEM, postchicken pox, abscess.
Neoplastic/paraneoplastic: primary/secondary
tumour, Anti-Hu/Yo
Vascular/degenerative: Strokes, MSA
Toxic/iatrogenic: alcohol, phenytoin

Parkinsonism-signs
Rest tremor, pin-rolling high amplitude, low
frequency
Rigidity-lead pipe
Rigidity- cog-wheel
Bradykinesia
Postural instability
Typical gait: Stooped posture, poor arm swing,
small short shuffling steps, festination, turning in
numbers and retropulsion.

Parkinsonism-plus: elicit;
Asymmetry
Vertical saccadic eye movements
Cerebellar signs
Postural hypotension, urinary incontinence,
impotence
Ask:
Drug history, family history, liver disease
Falls, Autonomic symptoms
Hx of hypoxic cerebral injury/ encephalitis
Mental state examination for cognitive impairment

Parkinsonismseverity/complications

Assess severity when walking the patient

Note any dyskinesia that may be present
Ask amount/types of medications he is on
Ask for complications such as falls, pneumonia.

Other movement disorders

Choreoathetosis: dance like irregular,
semi-purposeful, non-stereotypic
movements of the limbs, often bilateral;
patient looks restless.
If proximal and large amplitude: Ballismus

Choreoathetosis

Inherited: Huntington Chorea, Wilsons

disease, neuroacanthocytes, DRPLA, PKAN,
PKC
Infectious/inflammatory: Syndenhams,
Lupus, APS, Encephalitis
Metabolic-Endocrine: hyperglycemia,
hyperthyroidism, hypocalcaemia, pregnancy,
Vascular degenerative: stroke, DRPLA
Iatrogenic/toxic: drug induced (neurolepticstardive dyskinesia, dopa-dyskinesia in PD,
OCP, amphetamines), pump-chorea, postanoxic, kernicterus,
Neoplastic/paraneoplastic: NMDAR ab

Choreoathetosis-Rx

Tetrabenazine, dopamine antagonist

Benzhexol for tardive dyskinesia secondary to

neuroleptics

For PD dopa-dyskinesia: reduce L-dopa and

use long acting dopa antagonist