Upper/Lower Limb Neurological Examination Flashcards
What are the different types of generalised seizure?
- Absence: brief staring episode
- Myoclonic: extremely brief muscle contractions that look like jerky movements
- Tonic: tense contraction of muscles
- Clonic: rhythmic muscle contractions
- Tonic-clonic: initial muscle contraction (tonic phase) followed by rhythmic muscle contractions (clonic phase)
- Atonic: loss of muscle tone
List 3 causes of a bilateral upper motor neurone lesion
Bilateral upper motor neurone lesions can be remembered using the 3M’s:
MS
Motor neurone disease → normal sensation
Myelopathy – cord compression (e.g. due to cervical myelopathy, SOL, disc prolapse, paraspinal infection), trauma, transverse myelitis, syringomyelia, congenital → sensory-level/segmental sensory loss
Others – brainstem stroke, hereditary spastic paraplegia, cerebral palsy, HTLV-1, syphilis
What would be your differential diagnosis for a sensorimotor polyneuropathy?
Use ABCDE to list causes of a sensorimotor polyneuropathy:
Alcohol
B12/thiamine deficiency
Charcot-Marie-Tooth, Carcinomas (paraneoplastic)
Diabetes, Drugs (e.g. TB drugs, metronidazole/nitrofurantoin, vincristine/cisplatin, amiodarone)
Every vasculitis (e.g. SLE, RA, polyarteritis nodosa) and some infections (e.g. herpes zoster, HIV, leprosy, syphilis)
Which conditions may result in a unilateral upper motor neurone lesion?
Work down (brain to cord):
Intracranial – stroke, SOL → hemisensory loss
Brainstem – stroke, SOL → may be crossed signs
Spinal cord – MS, infarct/haemorrhage, SOL, disc prolapse, trauma, syringomyelia, congenital → sensory-level/segmental sensory loss
What are the causes and clinical features of a Brown-Sequard syndrome?
A Brown-Sequard syndrome is caused by damage to one half of the spinal cord. It is characterised by loss of power and proprioception on the ipsilateral side, and loss of pain and temperature on the contralateral side. This is because the spinothalamic tract decussates in the spine, whereas the other tracts decussate in the brainstem.
What is the differential diagnosis for a bilateral proximal weakness?
Bilateral proximal muscle weakness is usually caused by a myopathy.
The differential diagnosis can be remembered using DENIM:
Dystrophies – Becker’s/Duchenne, limb girdle, facioscapulohumeral (shoulder, face and truncal weakness)
Endocrinological – Cushing’s syndrome, hyper/hypothyroidism, diabetic amyotrophy (lower limbs)
Neuromuscular – myasthenia gravis (fatigable), Lambert–Eaton myasthenic syndrome
Inflammatory – dermato-/polymyositis, inclusion body myositis (proximal in legs but distal in arms), viral myositis
Metabolic/congenital/mitochondrial myopathies
Name some conditions associated with carpal tunnel syndrome. Name some other causes of a median nerve palsy.
Carpal tunnel syndrome may be associated with:
Pregnancy
Obesity
Rheumatoid arthritis
Local extrinsic pressure, e.g. ganglion, lipoma, fracture, haematoma
Endocrinological
Diabetes
Hypothyroidism
Acromegaly
Some other causes of median nerve palsy include: penetrating forearm injuries, pronator teres syndrome, mononeuritis multiplex
What are the causes of a radial nerve palsy?
Causes may include:
Trauma/compression at axilla (e.g. crutches, sleeping over chair, i.e. ‘Saturday night palsy’, stabbing injury)
Humeral shaft trauma (fracture)
Elbow trauma (fracture, dislocation, ganglion)
What are the clinical features that would suggest motor neurone disease during the upper limb clinical examination?
In motor neurone disease, the most common findings would be:
An exclusive motor deficit (no sensory abnormalities)
Classically a combination of LMN and UMN signs, for example in the upper limb exam you may see muscle wasting and fasciculations, but with increased tone and brisk reflexes
There may also be other clues, for example the patient may be in a wheelchair due to spastic paraparesis, and/or a speech abnormality (bulbar/pseudobulbar palsy)
Which hand muscles does the median nerve supply?
All thumb muscles except adductor pollicis – ‘LOAF’
Lateral two lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor Pollicis brevis
Which hand muscles does the ulnar nerve supply?
All intrinsic hand muscles except most of thumb:
Adductor pollicis
Lumbricals
‘Pad Dab’
Palmar interossei (adduct)
Dorsal Interossei (abduct)
Which hand muscles does the radial nerve supply?
Extensors
What can cause damage to the ulnar nerve and how would this present?
Causes
– Cubital tunnel syndrome
– Fractures
– Guyon’s canal
Presentation
– Numbness in the ring and little finger
– Reduced finger abduction and adduction
– Reduced adduction of the thumb
– Weak grip strength
– Muscle wasting
– Clawing of digits 4 and 5
What are the different management options for carpal tunnel syndrome?
Conservative
– The use of a night-time splint to hold the wrist in dorsiflexion
Medical
– Simple analgesia to relieve the pain
– Corticosteroid injections
Surgical
– Decompression surgery
What are some types of dysarthria?
Bulbar palsy = flaccid
Pseudobulbar palsy = spastic
Cerebellar = slurred, staccato (broken up into syllables, i.e. jerky), scanning (variability in pitch/volume)
Myasthenic = weak, quiet, fatigable
Please describe the difference between Broca’s and Wernicke’s aphasia. Damage to which areas of the cerebral cortex cause each of these aphasias?
Broca’s (expressive) aphasia:
This is a type of non-fluent aphasia
It is characterised by the inability to produce language, both spoken and written
Comprehension of speech is often intact
Caused by damage to the frontal lobe of the dominant hemisphere (often left)
Wernicke’s (receptive) aphasia:
This is a type of fluent aphasia
These patients have difficulty producing coherent sentences and understanding speech
The production of speech is intact
Caused by damage to the posterior superior temporal lobe
Which tests may be used to assess muscle fatiguability in patients with myasthenia gravis?
- Counting aloud 1 to 30 (speech will be clear initially but will become increasingly dysarthric)
- Single breath counting aloud 1 to 20 (may elicit dysarthria and dyspnoea)
- Sustained eye upgaze: ask patient to focus on your finger superiorly for 60+ seconds (results in ptosis)
- Test abduction of the arms and repeat after asking the patient to abduct/adduct repeatedly for 10-20 repetitions (power will be reduced after repetitions)
- Ask patient to stand from sitting and sit down again with their arm crossed. Ask them to repeat this up to 20 times (should exacerbate leg weakness)
How would a patient present if they had complete damage to cranial nerve X (Vagus nerve)?
The soft palate droops to one side
Loss of gag reflex
Dysphasia
Hoarse and nasal voice
Tachycardia
Gastroparesis/nausea and vomiting
Difficulties with GI transit and digestion
How would you differentiate between and bulbar and pseudobulbar palsy?
Bulbar palsy is due to LNM pathology, whereas pseudobulbar palsy is due to UMN pathology. There are therefore different signs:
Tongue wasting and fasciculations in bulbar palsy (spastic in pseudobulbar palsy)
Absent gag reflex in bulbar palsy (increased/normal in pseudobulbar palsy)
Speech in bulbar palsy = flaccid = indistinct with nasal twang
Speech in pseudobulbar palsy = spastic = monotonous, high- pitched, ‘Donald Duck’ dysarthria
Please list some causes of Parkinsonism
Parkinson’s disease
Vascular parkinsonism
Parkinson-plus syndromes
Other causes (e.g. drugs, Wilson’s disease)
What are the Parkinson-plus syndromes?
Progressive supranuclear palsy: vertical limitation, axial rigidity
Multi-system atrophy: cerebellar signs, autonomic problems
Corticobulbar degeneration
Dementia with Lewy bodies
What is the Parkinson’s disease tetrad?
Tremor
Rigidity
Bradykinesia
Postural instability
List some clinical features of Parkinson’s disease
Stooped posture
Hypomimia
Reduced arm swing
Shuffling gait
Slowness
Multiple falls
Anosmia
Postural hypotension
Depression
Restless leg syndrome
Which common class of drugs may cause drug-induced parkinsonism?
Antipsychotics. Their mechanism of action is dopamine depleting hence why the side effects can mimic Parkinson’s disease
What are the different functions of the cerebellum?
To maintain balance and posture
Coordinate movement including eye movements
Motor learning: fine tuning of movements that must be learnt
Please list some signs of cerebellar disease
DANISH:
Dysdiadochokinesia and Dysmetria
Ataxia
Nystagmus
Intention tremor
Speech abnormality (slurring/scanning/staccato)
Hypotonia
What are some causes of cerebellar disease?
MAVIS:
MS
Alcohol
Vascular
Inherited ataxias
Space occupying lesion
List some different causes of cerebellar ataxia based on their onset?
Acute
Vascular i.e., cerebral haemorrhage
Alcohol intoxication
Drugs including lithium and phenytoin
Infection i.e., cerebellitis
Sub-acute
Toxins such as lead, mercury, paint thinners
Inflammatory
Neoplastic or paraneoplastic
Chronic
Multiple systems atrophy
Friedreich ataxia
Chronic alcohol abuse
How could you differentiate sensory ataxia from cerebellar ataxia?
Romberg’s test can help differentiate:
This tests proprioception which is disrupted by a sensory disorder
Normally a patient who has a problem with proprioception can maintain balance by using their vision and vestibular function
In the Romberg’s test you remove the visual compensation and therefore expose the sensory ataxia
In cerebellar ataxia the patient would be ataxic prior to the test, or Romberg’s test would not positive as the problem is not sensory in nature
What is the classic speed of the pill-rolling tremor in Parkinson’s disease?
4-6Hz
Which medications can cause parkinsonism?
Antidopaminergic drugs include:
– Antipsychotics (typical > atypical)
– Methyldopa
– Some antiemetics (prochlorperazine, metoclopramide)
What are the clinical features of Wilson’s disease?
– Kayser–Fleischer rings
– Tremor/parkinsonism
– Psychiatric features (behavioural changes, anxiety, depression, psychosis)
– Signs of chronic liver disease (ascites, splenomegaly, spider naevi etc.)
– Signs of cardiomyopathy (oedema, raised JVP etc.)
What are the clinical features of upper and lower motor neuron lesions?
Upper motor neuron lesions:
– Increased tone
– Spasticity
– Weakness
– Brisk reflexes, upgoing plantar reflex
Lower motor neuron lesions:
– Wasting and fasciculation
– Hypotonia
– Weakness
– Reduced reflexes
Does multiple sclerosis cause upper or lower motor neuron lesions? Why?
Upper motor neuron lesions because multiple sclerosis causes destruction of the myelin sheaths of neurons of the central nervous system.
What is Lhermitte’s sign?
Electric shock-like sensation, which feels like it goes up/down spine, that occurs on flexion of the neck.
Root + nerve for shoulder ABduction
C5
Axillary
Root + nerve for elbow flexion
C5/6
Musculocutaneous
Root + nerve for elbow extension
C7
Radial
Root + nerve for wrist extension
C6
Radial
Root + nerve for finger extension
C7
Radial
Root + nerve for finger flexion
C8
Median + ulnar
Root + nerve for thumb abduction
T1
Median
Root + nerve for finger abduction
T1
Ulnar
Which movements are weak in UMN lesion of the arm?
Those marked with *
Tone, power, reflexes, plantars, co-ordination and other features in: LMN lesion
Tone, power, reflexes, plantars, co-ordination and other features in: UMN lesion
Tone, power, reflexes, plantars, co-ordination and other features in: extrapyramidal lesion
Tone, power, reflexes, plantars, co-ordination and other features in: cerebellar lesion
MRC grading of power (Neurology)
Sensory modalities carried in the spinal cord?
Pathology of spinal cord sensory tracts?
Features of syringomyelia?
Erb’s vs Klumpke’s palsy?
Root and nerve for hip flexion
L1/2
Femoral
Root and nerve for hip extension (push heel into bed)
L5/S1
Gluteal
Root and nerve for knee flexion
L5/S1
Sciatic
Root and nerve for knee extension
L3/4
Femoral
Root and nerve for ankle dorsiflexion
L4
Peroneal
Root and nerve for big toe extension
L5
Peroneal
Root and nerve for ankle plantarflexion
S1
Tibial
∆∆ paraparesis = bilateral leg weakness
∆∆ unilateral leg weakness
∆∆ peripheral neuropathy
Positive Romberg’s test?
SCDC (B12/folate deficiency)
Features of ALS?
∆∆ foot drop
Core features of Parkinsonism (TRAP)
Conditions with similar presentaitons to Parkinsonism?
Causes of Parkinsonism?
Long term complications of L-dopa therapy?
Treatments used in Parkinson’s disease?
∆∆ tremor
Features of benign essential tremor vs exaggerated physiological tremor
UMN vs LMN on examination
Pyramidal pattern on examination
Causes of pyramidal weakness
Pyramidal pattern of weakness
Spasticity vs rigidity
Velocity, Direction, Motor weakness, Pattern + Origin
UMN lesions: unilateral vs bilateral causes
LMN lesions: unilateral vs bilateral causes
Charcot Marie Tooth features + management
Proximal myopathy causes
Peripheral neuropathy ABCDE causes
Overview of spinal cord lesion patterns
Anterior spinal cord syndrome
Central spinal cord lesion
Posterior spinal cord lesion
Brown-Sequard spinal cord lesion
Parkinson’s associated symptoms
Examination findings in PD
First line agents for PD management
Missed doses of PD medications
Most common subtypes of MND
UMN and LMN signs seen in MND
Management of MND
Features seen in myasthenia gravis
Investigations in myasthenia gravis
Management of MG (also crisis)
Define MS + the subtypes/patterns
Auto-immune destruction of myelin sheath with plaques throughout brain and spinal cord = demyelinating UMN pathology
Symptoms of MS
Investigations for MS
Management of MS
Cerebellar signs
Investigation for cerebellar disease
Unilateral vs bilateral cerebellar disease
CNII (Optic) palsy
Presentation + Causes
CNIII (Oculomotor) palsy
Presentation + Causes
CNIV (Trochlear) palsy
Presentation + Causes
CNVI (Abducens) palsy
CNVII (facial) palsy
Bulbar (LMN) palsy
Presentation + Causes
Pseudobulbar palsy (UMN)
Presentation + Causes
