Neuro Flashcards
Cranial nerves general inspection
Speech abnormalities: may indicate glossopharyngeal or vagus nerve pathology.
Facial asymmetry: suggestive of facial nerve palsy.
Eyelid abnormalities: ptosis may indicate oculomotor nerve pathology.
Pupillary abnormalities: mydriasis occurs in oculomotor nerve palsy.
Strabismus: may indicate oculomotor, trochlear or abducens nerve palsy.
Limbs: pay attention to the patient’s arms and legs as they enter the room and take a seat noting any abnormalities (e.g. spasticity, weakness, wasting, tremor, fasciculation) which may suggest the presence of a neurological syndrome).
Medical paraphernalia of neuro disease
Walking aids: gait issues are associated with a wide range of neurological pathology including Parkinson’s disease, stroke, cerebellar disease and myasthenia gravis.
Hearing aids: often worn by patients with vestibulocochlear nerve issues (e.g. Ménière’s disease).
Visual aids: the use of visual prisms or occluders may indicate underlying strabismus.
Prescriptions: prescribing charts or personal prescriptions can provide useful information about the patient’s recent medications.
Causes of anosmia
Mucous blockage of the nose: preventing odours from reaching the olfactory nerve receptors.
Head trauma: can result in shearing of the olfactory nerve fibres leading to anosmia.
Genetics: some individuals have congenital anosmia.
Parkinson’s disease: anosmia is an early feature of Parkinson’s disease.
COVID-19: transient anosmia is a common feature of COVID-19.
Causes of decreased visual acuity
Refractive errors
Amblyopia
Ocular media opacities such as cataract or corneal scarring
Retinal diseases such as age-related macular degeneration
Optic nerve (CN II) pathology such as optic neuritis
Lesions higher in the visual pathways
Relative afferent pupillary defect
When the afferent limb in one of the optic nerves is damaged, partially or completely, both pupils will constrict less when light is shone into the affected eye compared to the healthy eye. The pupils, therefore, appear to relatively dilate when swinging the torch from the healthy to the affected eye.
sign of retinal damage: optic neuritis, CRVO, CRAO, larger retinal detachment, unilateral advanced glaucoma, compression secondary to tumour or abscess.
Unilateral efferent defect
commonly caused by extrinsic compression of the oculomotor nerve, resulting in the loss of the efferent limb of the ipsilateral pupillary reflexes. As a result, the ipsilateral pupil is dilated and non-responsive to light entering either eye (due to loss of ciliary sphincter function). The consensual light reflex in the unaffected eye would still be present as the afferent pathway (i.e. optic nerve) of the affected eye and the efferent pathway (i.e. oculomotor nerve) of the unaffected eye remain intact.
Colour vision deficiencies
Optic neuritis: results in a reduction of colour vision (typically red).
Vitamin A deficiency
Chronic solvent exposure
Visual neglect/inattention
= deficit in awareness in one side of visual field
usually parietal lobe injury after stroke
differentiate between true visual field loss (optic nerve) and inattention (cerebral hemisphere)
Visual extinction
patient can’t identify one of the moving fingers when a finger on both hands is wiggling simultaneously. They can, however, identify each of them when they’re wiggled individually.
Visual field defects
bitemporal hemianopia
homonymous field defects
scotoma
monocular vision loss
Bitemporal hemianopia
loss of the temporal visual field in both eyes resulting in central tunnel vision.
result of optic chiasm compression by a tumour (e.g. pituitary adenoma, craniopharyngioma).
Homonymous field defects
affect the same side of the visual field in each eye and are commonly attributed to stroke, tumour, abscess (i.e. pathology affecting visual pathways posterior to the optic chiasm). These are deemed hemianopias if half the vision is affected and quadrantanopias if a quarter of the vision is affected.
Scotoma
an area of absent or reduced vision surrounded by areas of normal vision. There is a wide range of possible aetiologies including demyelinating disease (e.g. multiple sclerosis) and diabetic maculopathy.
Monocular vision loss
total loss of vision in one eye secondary to optic nerve pathology (e.g. anterior ischaemic optic neuropathy) or ocular diseases (e.g. central retinal artery occlusion, total retinal detachment).
Causes of ptosis
Oculomotor nerve pathology
Horner’s syndrome
Neuromuscular pathology (e.g. myasthenia gravis)
Oculomotor nerve palsy
The oculomotor nerve supplies all extraocular muscles except the superior oblique (CNIV) and the lateral rectus (CNVI). Oculomotor palsy (a.k.a. ‘third nerve palsy’), therefore, results in the unopposed action of both the lateral rectus and superior oblique muscles, which pull the eye inferolaterally. As a result, patients typically present with a ‘down and out’ appearance of the affected eye.
Oculomotor nerve palsy can also cause ptosis (due to a loss of innervation to levator palpebrae superioris) as well as mydriasis due to the loss of parasympathetic fibres responsible for innervating to the sphincter pupillae muscle.
Trochlear nerve palsy (CN IV)
innervates is the superior oblique muscle. As a result, trochlear nerve palsy (‘fourth nerve palsy’) typically results in vertical diplopia when looking inferiorly, due to loss of the superior oblique’s action of pulling the eye downwards. Patients often try to compensate for this by tilting their head forwards and tucking their chin in, which minimises vertical diplopia. Trochlear nerve palsy also causes torsional diplopia (as the superior oblique muscle assists with intorsion of the eye as the head tilts). To compensate for this, patients with trochlear nerve palsy tilt their head to the opposite side, in order to fuse the two images together.
Abducens nerve palsy (CN VI)
The abducens nerve (CN VI) innervates the lateral rectus muscle. Abducens nerve palsy (‘sixth nerve palsy’) results in unopposed adduction of the eye (by the medial rectus muscle), resulting in a convergent squint. Patients typically present with horizontal diplopia which is worsened when they attempt to look towards the affected side.
Facial nerve palsy
Facial nerve palsy caused by a lower motor neuron lesion presents with weakness of all ipsilateral muscles of facial expression, due to the loss of innervation to all muscles on the affected side. The most common cause of lower motor neuron facial palsy is Bell’s palsy.
Facial nerve palsy caused by an upper motor neuron lesion also presents with unilateral facial muscle weakness, however, the upper facial muscles are partially spared because of bilateral cortical representation (resulting in forehead/frontalis function being somewhat maintained). The most common cause of upper motor neuron facial palsy is stroke.
Rinne’s test
Normal result: air conduction > bone conduction (Rinne’s positive)
Sensorineural deafness: air conduction > bone conduction (Rinne’s positive) – due to both air and bone conduction being reduced equally
Conductive deafness: bone conduction > air conduction (Rinne’s negative)
Weber’s test
Normal: sound is heard equally in both ears.
Sensorineural deafness: sound is heard louder on the side of the intact ear.
Conductive deafness: sound is heard louder on the side of the affected ear.
Conductive vs sensorineural hearing loss
Conductive hearing loss occurs when sound is unable to effectively transfer at any point between the outer ear, external auditory canal, tympanic membrane and middle ear (ossicles). Causes of conductive hearing loss include excessive ear wax, otitis externa, otitis media, perforated tympanic membrane and otosclerosis.
Sensorineural hearing loss occurs due to dysfunction of the cochlea and/or vestibulocochlear nerve. Causes of sensorineural hearing loss include increasing age (presbycusis), excessive noise exposure, genetic mutations, viral infections (e.g. cytomegalovirus) and ototoxic agents (e.g. gentamicin).
Hypoglossal nerve palsy
causes atrophy of the ipsilateral tongue and deviation of the tongue when protruded towards the side of the lesion. This occurs due to the overaction of the functioning genioglossus muscle on the unaffected side of the tongue.
Vagus nerve lesion
asymmetrical elevation of palate
uvula deviation away from lesion
inability to close glottis (weak cough)
absence of gag reflex (+glossopharyngeal)
change to voice quality (+glossopharyngeal)
To complete CN exam
Full history
Full neurological examination including the upper and lower limbs.
FUNDOSCOPY
Neuroimaging (e.g. MRI head): if there are concerns about space-occupying lesions or demyelination.
Formal hearing assessment (including pure tone audiometry): if there are concerns about vestibulocochlear nerve function.
UMN lesion signs
Inspection:
no fasciculations or muscle wasting (maybe some disuse atrophy)
Pronator drift in UL
Increased tone (spasticity or rigidity)
Power = pyramidal weakness pattern (extensors weaker than flexors in arms, vice versa in legs)
Hyperreflexia
LMN lesion signs
Inspection:
Wasting and fasciculation of muscles
No pronator drift in arms
Decreased tone or normal
Weakness pattern depends on cause (eg proximal = muscles, distal = peripheral neuropathy)
Reduced or absent reflexes
Chorea
brief, semi-directed, irregular movements that are not repetitive or rhythmic but appear to flow from one muscle to the next. Patients with Huntington’s disease typically present with chorea
Myoclonus
brief, involuntary, irregular twitching of a muscle or group of muscles. All individuals experience benign myoclonus on occasion (e.g. whilst falling asleep) however persistent widespread myoclonus is associated with several specific forms of epilepsy (e.g. juvenile myoclonic epilepsy).
Tardive dyskinesia
involuntary, repetitive body movements which can include protrusion of the tongue, lip-smacking and grimacing. This condition can develop secondary to treatment with neuroleptic medications including antipsychotics and antiemetics.
Pseudoathetosis
abnormal writhing movements (typically affecting the fingers) caused by a failure of proprioception.
Hypomimia
a reduced degree of facial expression associated with Parkinson’s disease.
Ophthalmoplegia
weakness or paralysis of one or more extraocular muscles responsible for eye movements. Ophthalmoplegia can be caused by a wide range of neurological disorders including multiple sclerosis and myasthenia gravis.
Spasticity vs rigidity
Spasticity is associated with pyramidal tract lesions (e.g. stroke) and rigidity is associated with extrapyramidal tract lesions (e.g. Parkinson’s disease).
Spasticity is “velocity-dependent”, meaning the faster you move the limb, the worse it is. There is typically increased tone in the initial part of the movement which then suddenly reduces past a certain point (known as “clasp knife spasticity”). Spasticity is also typically accompanied by weakness.
Rigidity is “velocity independent” meaning it feels the same if you move the limb rapidly or slowly. There are two main sub-types of rigidity:
Cogwheel rigidity involves a tremor superimposed on the hypertonia, resulting in intermittent increases in tone during movement of the limb. This subtype of rigidity is associated with Parkinson’s disease.
Lead pipe rigidity involves uniformly increased tone throughout the movement of the muscle. This subtype of rigidity is typically associated with neuroleptic malignant syndrome.
Shoulder abduction nerve root and muscles
C5 (axillary nerve)
deltoid and supraspinatus
Shoulder adduction nerve root and muscles
C6/7 (thoracodorsal nerve)
Teres major, latissimus dorsi, pectoralis major
Elbow flexion nerve root and muscles
C5/6 (musculocutaneous and radial nerve)
bicep brachii, coracobrachialis, brachialis
Elbow extension nerve root and muscles
C7 (radial nerve)
triceps brachii
Wrist extension nerve root and muscles
C6 (radial nerve)
extensors of wrist
Wrist flexion nerve root and muscles
C6/7 (median and ulnar nerve)
Flexors of wrist
Finger extension nerve root and muscles
C7 (radial)
extensor digitorum
Finger abduction nerve root and muscles
T1 (ulnar)
first dorsal interosseous (FDI) and abductor digiti minimi (ADM)
Thumb abduction nerve root and muscles
T1 (median)
abductor pollicis brevis
MRC power scale
0 No contraction
1 Flicker or trace of contraction
2 Active movement, with gravity eliminated
3 Active movement against gravity
4 Active movement against gravity and resistance
5 Normal power
Biceps reflex (root)
C5/6
Supinator reflex root
C5/6
Triceps reflex root
C7
UL dermatomes
C5: the lateral aspect of the lower edge of the deltoid muscle (known as the “regimental badge”).
C6: the palmar side of the thumb.
C7: the palmar side of the middle finger.
C8: the palmar side of the little finger.
T1: the medial aspect antecubital fossa, proximal to the medial epicondyle of the humerus.
Spinothalamic tracts
Pin-prick (pain)
Temperature
Dorsal columns
Vibration sense (128 Hz)
Joint proprioception
Sensory loss patterns
Mononeuropathies
Peripheral neuropathy
Radiculopathy
Spinal cord damage
Thalamic lesions
Myopathies
Mononeuropathies
result in a localised sensory disturbance in the area supplied by the damaged nerve.
Peripheral neuropathy
typically causes symmetrical sensory deficits in a ‘glove and stocking’ distribution in the peripheral limbs. The most common causes of peripheral neuropathy are diabetes mellitus and chronic alcohol excess.
Radiculopathy
occurs due to nerve root damage (e.g. compression by a herniated intervertebral disc), resulting in sensory disturbances in the associated dermatomes.
Spinal cord damage
results in sensory loss both at and below the level of involvement in a dermatomal pattern due to its impact on the sensory tracts running through the cord.
Thalamic lesions
(e.g. stroke) result in contralateral sensory loss.
Myopathies
often involve symmetrical proximal muscle weakness.
Coordination (cerebellar pathology)
Dysmetria: refers to a lack of coordination of movement. Clinically this results in the patient missing the target by over/undershooting.
Intention tremor: a broad, coarse, low-frequency tremor that develops as a limb reaches the endpoint of a deliberate movement. Clinically this results in a tremor that becomes apparent as the patient’s finger approaches yours. Be careful not to mistake an action tremor (which occurs throughout the movement) for an intention tremor.
Dysdiadochokinesia: slow and irregular movements
=ipsilateral cerebellar lesion
Gait inspection
Stance: observe the patient’s posture for asymmetries which may indicate weakness, abnormalities of proprioception or cerebellar pathology.
Base: a broad-based ataxic gait is typically associated with midline cerebellar pathology (e.g. a lesion in multiple sclerosis or degeneration of the cerebellar vermis secondary to chronic alcohol excess).
Stability: a staggering, slow and unsteady gait is typical of cerebellar pathology. In unilateral cerebellar disease, patients will veer towards the side of the lesion.
Arm swing: often absent or reduced in Parkinson’s disease (typically unilateral initially).
Stride length and step height: small, shuffling steps are characteristic of Parkinson’s disease. High-stepping may indicate the presence of foot drop.
Turning: patients with cerebellar disease will find the turning manoeuvre particularly difficult.
Tandem gait (heel-to-toe)
Tandem gait is particularly sensitive at identifying dysfunction of the cerebellar vermis (e.g. alcohol-induced cerebellar degeneration). Difficulties with heel-to-toe walking may also suggest weakness of the flexors muscles of the leg or sensory ataxia.
Gait abnormalities
Ataxic gait
Parkinsonian
High-stepping
Waddling
Hemiparetic
Spastic paresis
Ataxic gait
broad-based, unsteady and associated with either cerebellar pathology or sensory ataxia (e.g. vestibular or proprioceptive dysfunction). In the context of proprioceptive sensory ataxia, patients typically watch their feet intently to compensate for the proprioceptive loss. If a cerebellar lesion is present the patient may veer to the side of the lesion.
Parkinsonian gait
small, shuffling steps, stooped posture and reduced arm swing (initially unilateral). The patient will require several small steps to turn around. The gait appears rushed (festinating) and may get stuck (freeze). Hand tremor may also be noticeable.
High-stepping gait
can be unilateral or bilateral and is typically caused by foot drop (weakness of ankle dorsiflexion). The patient also won’t be able to walk on their heel(s).
Waddling gait
shoulders sway from side to side, legs lifted off ground with the aid of tilting the trunk. Waddling gait is commonly caused by proximal lower limb weakness (e.g. myopathy).
Hemiparetic gait
one leg held stiffly and swings round in an arc with each stride (circumduction). This type of gait is commonly associated with individuals who have had a stroke.
Spastic paresis
similar to hemiparetic gait but bilateral, with both legs stiff and circumducting. The patient’s feet may be inverted and “scissor”. This type of gait is typically associated with hereditary spastic paraplegia.
Romberg’s test
Romberg’s test is based on the premise that a patient requires at least two of the following three senses to maintain balance whilst standing:
Proprioception: the awareness of one’s body position in space.
Vestibular function: the ability to know one’s head position in space.
Vision: the ability to see one’s position in space.
Romberg’s test involves removing the sense of vision by asking the patient to close their eyes. As a result, if the patient has a deficit in proprioception or vestibular function they will struggle to remain standing without visual input.
Causes of proprioceptive dysfunction
joint hypermobility (e.g. Ehlers-Danlos syndrome)
B12 deficiency
Parkinson’s disease and ageing (known as presbypropria).
Causes of vestibular dysfunction
vestibular neuronitis and Ménière’s disease.
Hip flexion nerve root and muscles
L1/2
iliopsoas
Hip extension nerve root and muscles
L5/S1/S2 (inferior gluteal)
gluteus maximus
Knee flexion nerve root and muscles
S1 (sciatic)
hamstrings
Knee extension nerve root and muscles
L3/4 (femoral)
quadriceps
Ankle dorsiflexion nerve root and muscles
L4/5 (deep peroneal)
tibialis anterior
Ankle plantarflexion nerve root and muscles
S1/2 (tibial)
gastrocnemius, soleus
Big toe extension nerve root and muscles
L5 (deep peroneal)
extensor hallucis longus
Knee jerk reflex root
L3/4
Ankle jerk reflex root
S1/2
Plantar reflex root
L5/S1
(use orange stick)
Babinski sign
extension of the big toe and spread of the other toes (suggestive of an upper motor neuron lesion).
LL dermatomes
L1: inguinal region and the very top of the medial thigh
L2: middle and lateral aspect of the anterior thigh
L3: medial aspect of the knee
L4: medial aspect of the lower leg and ankle
L5: dorsum and medial aspect of the big toe
S1: dorsum and lateral aspect of the little toe
