Neuro

Question 1

What is a hemiplegic gait?

Answer 1

Asymmetrical gait; one limb is normal while the affected limb is stiff (spastic)
Affected limb held in extension (knee extension and foot plantar flexion) with feet inverted
Toes on the affected side may drag on the floor due to fixed ankle plantarflexion and knee extension lengthening the leg
Affected leg swings around (i.e. circumducts) during the swing phase to prevent the feet from dragging

Question 2

What are the clinical features associated with a hemiplegic gait?

Answer 2

Other signs of upper motor neuron pyramidal weakness are typically found on the affected side (upper and lower limb):

Increased tone with clasp-knife spasticity
Hyperreflexia with or without clonus
Upgoing plantars (i.e. positive Babinski)
Reduced power
The upper limb may have flexor posturing of elbows and wrist with shoulders and fingers in adduction

Sensory deficit – the pattern of sensory loss is important to give clues to the cause

Question 3

What are the differential diagnosis for a hemiplegic gait?

Answer 3

Unilateral upper motor neuron lesion:
Unilateral brain lesion on the contralateral side of the affected limb (most likely cause):
Ischaemic/haemorrhagic stroke
Brain tumour
Trauma
Demyelination (e.g. multiple sclerosis)
Space-occupying lesion

Hemisection of the spinal cord (Brown-Sequard syndrome) on the ipsilateral side of the affected limb (rarer):
Prolapsed intervertebral disc
Spinal spondylosis
Spinal tumour
Demyelination
Spinal infarct

Question 4

What are the key points regarding a hemiplegic gait diagnosis?

Answer 4

Hemisection of spinal cord causes ipsilateral loss of proprioception and vibration sensation and contralateral loss of pain and temperature sensation
Complete transection of the spinal cord would normally give a diplegic gait
Spinal cord lesions usually cause impairment in sensation, whereas brain lesions may leave sensation intact

Question 5

What is a diplegic gait?

Answer 5

Findings are similar to hemiplegic gait but bilateral in nature
Limbs are stiff and held in extension with feet inverted and internally rotated
Hips are drawn together due to excessive adductor tone
Legs are forced together due to spasticity which results in leg overlap when walking
Circumduction of both legs during the swing phase
Symmetrical movement of lower limb

Question 6

What are the clinical features associated with a diplegic gait?

Answer 6

Other signs of an upper motor neuron pyramidal deficit on the affected side (upper and lower limb):

Increased tone with clasp-knife spasticity
Reduced power
Hyperreflexia with or without clonus
Upgoing plantars (positive Babinski)
The upper limb may have flexor posturing of elbows and wrist with shoulders and fingers in adduction
NB: If upper motor neuron signs are present in the upper limb, the site of the lesion must be at or above the level of the cervical spine

Question 7

What are the differential diagnoses for a diplegic gait?

Answer 7

Spinal cord lesion (sensation usually affected):
Prolapsed intervertebral disc
Spinal spondylosis
Spinal tumour
Transverse myelitis
Spinal infarct
Syringomyelia
Hereditary spastic paraparesis

Bilateral brain lesion:
Cerebral palsy
Multiple sclerosis
Bilateral brain infarcts
Midline tumour (e.g. paraspinal meningioma)
Motor neuron disease
Associated with lower motor neuron findings

Question 8

What is a parkinsonian gait?

Answer 8

‘Festinant gait’ – short-stepping, shuffling
Minimal arm swing (an early feature of a Parkinsonian gait)
Difficulty/hesitancy when asked to start, turn around and stop walking
Difficulty initiating new movements
Stooped posture
Hypomimia (expressionless face)
Hypokinetic gait

Question 9

What are the clinical features associated with a Parkinsonian gait?

Answer 9

Idiopathic Parkinson’s disease classically presents with a triad of:
Tremor
Rigidity
Bradykinesia

There may be other associated features including:
Cogwheel rigidity
Asymmetrical tremor (typically pin-rolling)
Bradykinesia
Difficulty getting up from a seated position

Question 10

What are the differential diagnoses for a parkinsonian gait?

Answer 10

Vascular Parkinson’s disease
Dementia with Lewy bodies
Parkinson’s plus syndromes
Multisystem atrophy – associated with autonomic and cerebellar signs
Progressive supranuclear palsy – associated with vertical gaze palsies
Drug-induced (dopamine antagonists)
Antipsychotics
Antiemetics
Dementia pugilistica

Question 11

What is an ataxic gait?

Answer 11

Broad-based
Unsteady
Foot stamping
May require support with a walking frame
If unilateral cerebellar lesion present, the patient may veer towards the side of the lesion
Heel-toe walking may help elicit ataxia if gait initially appears normal

Question 12

What are the clinical features associated with an ataxic gait?

Answer 12

Ataxic gait implies either cerebellar, vestibular or sensory impairment.
If cerebellar disease is the cause, other signs of cerebellar disease may be present. If the cerebellar lesion is unilateral then the signs are present on the same side of the lesion.

Cerebellar ataxia:
Nystagmus (on the affected side of the lesion if unilateral cerebellar lesion)
Ataxic dysarthria
Dysmetria (i.e. past-pointing or under-shooting)
Intentional tremor (on the affected side of the lesion if unilateral cerebellar lesion)
Dysdiadokokinesia (on the affected side of the lesion if unilateral cerebellar lesion)

Sensory ataxia:
Sensory neuropathy gives the appearance of an ataxic gait due to impaired limb sensation
Signs include:
Positive Romberg’s sign
Impaired proprioception (joint position sense)
Impaired vibration sense
The absence of other cerebellar signs (e.g. dysmetria, nystagmus, dysarthria etc)

Vestibular ataxia:
Vestibular disturbance can give a gait similar to an ataxic gait
Associated with vertigo, nausea and vomiting

Question 13

What are the differential diagnoses for an ataxic gait?

Answer 13

Unilateral cerebellar disease (unilateral cerebellar findings):
Ischaemic (posterior circulation infarct) or haemorrhagic stroke – vascular events produce hyperacute symptoms
Space-occupying lesion

Bilateral cerebellar disease (giving bilateral cerebellar findings):
Multiple sclerosis
Alcoholism
B12 deficiency
Drugs: phenytoin, carbamazepine, barbiturates, lithium
Genetic: Frederich’s Ataxia, spinocerebellar ataxia, ataxic telangiectasia
Paraneoplastic disease
Multi-systems atrophy – associated with Parkinsonian and autonomic features

Question 14

What is a neuropathic gait?

Answer 14

“Foot drop”- There is weakness of dorsiflexion, so the foot drops and toes drag during swing phase
To prevent the toes from dragging on the floor, the knee and hip flexes excessively, thereby creating a “high stepping” gait
Feet stamp on the floor

Question 15

What are the clinical features associated with neuropathic gait?

Answer 15

Ankle-foot orthoses:
Aid to keep ankle fixed in dorsiflexion

Unilateral foot drop with sensory impairment:
Common peroneal nerve disease- usually with a sensory loss on the dorsum of the foot and lateral calf
L5 nerve route disease- usually with sensory loss in the distribution of the L5 dermatome

Bilateral distal muscle weakness with foot drop:
Seen in peripheral neuropathies or motor neurone disease
The appearance of pes cavus and “inverted champagne bottle calf” are features of hereditary motor and sensory neuropathies

Reflexes:
Reduced or absent in peripheral neuropathies
Brisk with upgoing plantars and fasciculations (a mixture of upper and lower motor neurone signs) in motor neurone disease

Question 16

What are the differential diagnoses for a neuropathic gait?

Answer 16

Foot drop implies weakness of the muscles of ankle dorsiflexion (tibialis anterior) supplied by the common peroneal nerve (L4, L5 and S1 nerve root).
This is due to either:
Isolated common peroneal nerve palsy
L5 radiculopathy (weakened foot inversion)
OR
Part of generalized polyneuropathy involving multiple nerves
NB: Unilateral foot drop with no other muscles or nerves involved suggests an isolated neuropathy- common peroneal palsy or L5 radiculopathy, and not a polyneuropathy. Common peroneal nerve palsy or L5 radiculopathy is usually unilateral, but can be bilateral.

Common peroneal nerve palsy (preserved foot inversion):
Trauma or compression – especially as the nerve passes around the head of the fibula (e.g. head of fibular fracture or plaster cast)

A bilateral foot drop with other neurological features (muscle wasting, reduced reflexes, impaired sensation in a distribution outside common peroneal nerve/L5 dermatome, and weakness in muscles other than ankle dorsiflexors) is seen in more diffuse disease:
Polyneuropathies:
Diabetic neuropathy
Hereditary motor and sensory neuropathies (Charcot-Marie Tooth disease is a type of hereditary motor and sensory neuropathy)
Vasculitis
Guillain-Barré syndrome
Motor neurone disease: associated with upper and lower motor neurone findings

Question 17

What is a sensory gait?

Answer 17

Caused by peripheral sensory nerve impairment
The patient cannot sense where the foot is (i.e. impaired proprioception), nor when the foot hits the ground. To compensate the patient slams their foot on the ground in order to sense when the foot has hit the ground.
Gait may also appear ataxic with sensory impairment (sensory ataxia)

Question 18

What are the clinical features associated with a sensory gait?

Answer 18

Romberg’s test positive:
Balance is maintained by vestibular input, visual input and proprioception (joint position sense). We need two out of three to be intact in order to maintain balance. In a healthy person when visual input stops (closed eyes), we rely on vestibular and proprioception (two inputs) to maintain balance.
In a patient with peripheral sensory impairment (proprioception impaired), when the eyes are closed (visual input removed), they only have their vestibular input to maintain balance. One input is not enough and so the patient becomes unsteady.
Stomping is exacerbated in the dark
Impaired sensation to the feet must be present in order to confirm the diagnosis
Usually due to diseases affecting the spinal dorsal columns (dorsal column disease causes impaired proprioception and vibration sense)

Other features of a peripheral neuropathy may be present:
Diminished ankle reflexes
Peripheral motor weakness (causing a neuropathic gait with foot drop)

Features of sub-acute degeneration of the cord may be seen in B12 deficiency:
Diminished proprioception and vibration sense with absent ankle reflexes
Exaggerated knee reflex
Upgoing (positive) Babinski reflex

Question 19

What are the differential diagnoses of a sensory gait?

Answer 19

Dorsal column disease:
B12 deficiency
Tabes dorsalis (syphilis)

Peripheral nerve disease:
Diabetes
Vasculitis
B12 deficiency
Hereditary motor and sensory neuropathies (e.g. Charcot-Marie Tooth Disease)
Guillain-Barré syndrome
Post-infection

Question 20

What is a myopathic/Trendelenberg/waddling gait?

Answer 20

Hip abductors are weak so they are unable to contract and stabilize the pelvis during the stance phase. Therefore, the pelvis tilts down (instead of staying horizontal) towards the leg in swing phase.
The body compensates to prevent the swinging foot from dragging by:
Laterally flexing the torso away from the leg in swing phase- this draws the pelvis and leg up off the floor, and gives the characteristic ‘waddling’ appearance
Circumducting the leg

Question 21

What are the clinical features associated with a myopathic/Trendelenberg/waddling gait?

Answer 21

Trendelenburg’s sign positive:
When the patient stands on one leg, the pelvis drops towards the contralateral side

Signs of proximal myopathy:
Difficulty standing from a seated position without using arms
Difficulty standing from a squat or sitting up from a lying position

Evidence of systemic disease or a muscular dystrophy causing proximal myopathy

Question 22

What are the differential diagnoses of a myopathic/Trendelenberg/waddling gait?

Answer 22

Any cause of a proximal myopathy (there are many), including:
Systemic disease
Hyperthyroidism
Hypothyroidism
Cushing’s syndrome
Acromegaly
Polymyalgia rheumatica
Polymyositis
Dermatomyositis

Muscular dystrophies
Duchenne’s muscular dystrophy
Becker’s muscular dystrophy
Myotonic dystrophy

Question 23

What would a lesion at the optic nerve lead to?

Answer 23

Total ipsilateral blindness

Question 24

What would a lesion at the optic chiasm lead to?

Answer 24

Bipolar hemianopia

Question 25

What would a lesion at the optic tract lead to?

Answer 25

Ipsilateral nasal hemianopia

Question 26

What would a lesion at the optic radiation lead to?

Answer 26

Contralateral homonymous hemianopia

Question 27

What would a lesion at the lateral geniculate nucleus lea to?

Answer 27

Contralateral homonymous hemianopia with macular sparing

Question 28

What can cause an ischaemic stroke?

Answer 28

Embolism: An embolus from somewhere else in the body (e.g. the heart) causes obstruction of a cerebral vessel, resulting in hypoperfusion to the area of brain the vessel supplies.
Thrombosis: A blood clot forms locally within a cerebral vessel (e.g. due to atherosclerotic plaque rupture).
Systemic hypoperfusion: Reduced blood supply to the entire brain secondary to systemic hypotension (e.g. cardiac arrest).
Cerebral venous sinus thrombosis: Blood clots form in the veins that drain the brain, resulting in venous congestion and hypoxia which damages brain tissue.

Question 29

What are the types of haemorrhagic stroke?

Answer 29

Intracerebral haemorrhage: Bleeding within the brain itself secondary to a ruptured blood vessel.
Intraparenchymal (bleeding within the brain tissue)
Intraventricular (bleeding within the ventricles)
Subarachnoid haemorrhage: Bleeding that occurs outside of the brain tissue, between the pia mater and arachnoid mater.

Question 30

What classification can be used to classify ischaemic strokes?

Answer 30

Bamford classification

Question 31

What are the subtypes of ischaemic strokes according to the Bamford classification?

Answer 31

Total anterior circulation stroke (TACS)
Partial anterior circulation stroke (PACS)
Posterior circulation syndrome (POCS)
Lacunar syndrome (LACS)

Question 32

What is a total anterior circulation stroke?

Answer 32

A total anterior circulation stroke (TACS) involves a large cortical stroke affecting the areas of the brain supplied by both the middle and anterior cerebral arteries.

All three of the following need to be present for a diagnosis of TACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Question 33

What is a partial anterior circulation stroke?

Answer 33

A partial anterior circulation stroke (PACS) is a less severe form of TACS, in which only part of the anterior circulation has been compromised.

Two of the following need to be present for a diagnosis of PACS:
Unilateral weakness (and/or sensory deficit) of the face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction (dysphasia, visuospatial disorder)

Question 34

What is posterior circulation syndrome?

Answer 34

A posterior circulation syndrome (POCS) involves damage to the area of the brain supplied by the posterior circulation (e.g. cerebellum and brainstem).

One of the following need to be present for a diagnosis of POCS:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

Question 35

What is a lacunar syndrome?

Answer 35

A lacunar syndrome (LACS) involves a subcortical stroke that occurs secondary to small vessel disease. There is no loss of higher cerebral functions (e.g. dysphasia).

One of the following needs to be present for a diagnosis of LACS:
Pure sensory stroke
Pure motor stroke
Senori-motor stroke
Ataxic hemiparesis