neurology Flashcards
spastic gait
Pace shortens and narrow base is maintained
more pronounced in extensor muscles causing stiff and slow walking.
parkinsonian gait
posture is stooped and arm swing reduced
gait becomes hesitant with shorter rapid steps which slows down to a shuffle in advanced disease
Describe the presentation of cerebellar ataxia
In lateral cerebellar disease - stance becomes broad-based and uncoordinated
In midline (vermis) cerebellar disease - truncal ataxia leads to a tendency to fall backwards or sideways
Outline the effect of gait occurring in sensory ataxia?
Loss of proprioception - leading to a broad-based, high-stepping gait
syncope
a short duration (usually 20-30s) of loss of consciousness caused by a global reduction in cerebral blood flow
components of motor axis
motor cortex
corticospinal tracts
anterior horn cells
spinal nerve roots
peripheral nerves
neuromuscular junctions
muscle fibres
components of pyramidal system
corticospinal tract
corticobulbar tract
upper motor neurone lesion features
signs on opposite side to lesion
no muscle wasting
spasticity (+/- clonus)
hyperreflexia
extensor plantar response (Babinski signs)
lower motor neurone lesion features
signs on same side as the lesion
fasciculations
wasting
hypotonia
hyporeflexia
two patterns of clinical features which occur in an upper motor neurone lesion?
hemiparesis and paraparesis
hemiparesis
weakness of limbs on one side (usually caused by a lesion within the brain or brainstem e.g. a stroke)
paraparesis
weak legs.
indicative of bilateral damage to the corticospinal tracts (most commonly due to lesions below the T1 spinal level
lower motor neurone
motor pathway from anterior horn cell or cranial nerve via a peripheral nerve to the motor endplate
most common causes of a lower motor neurone lesion
anterior horn cells lesions e.g. motor neurone disease
spinal root lesion e.g. cervical and lumbar disc lesions
peripheral nerve lesions e.g. trauma, compression etc.
most common disease of the neuromuscular junction?
Myaesthenia Gravis
elevation of what plasma muscle enzyme indicates muscle disease?
creatine kinase
sensory peripheral nerves carry information from the dorsal root ganglion to the brain via three main pathways, what are they?
posterior columns
spinothalamic tracts
spinocerebellar tract
sensory modalities transmitted via the posterior columns
vibration
two-point discrimination
light touch
sensory modalities transmitted via the spinothalamic tract
pain
temperature
route of the posterior column
fibres ascend uncrossed to the gracile and cuneate nuclei in the medulla.
axons from the second-order neurones cross the midline to form the medial lemniscus and pass to the thalamus
route of the spinothalamic tract
fibres synapse in dorsal horn of the cord, cross the cord at that spinal level and ascend to the thalamus
sensory modalities are transmitted via the spinocerebellar tract?
proprioception
route of the spinocerebellar tract
does not decussate i.e. innervates the ipsilateral side of the body
The quality and distribution of the symptoms depend on the site of the lesion. Outline the potential sites of nerve lesions and their corresponding characteristics?
Peripheral nerve lesions - symptoms in the distribution of the affected nerve
Spinal root lesions - symptoms referred to affected dermatome
Spinal cord lesions - Symptoms are evident below the level of the lesion
Pontine lesions - Loss of all possible sensation on the opposite side of the lesion
Thalamic lesions - A rare cause of complete contralateral sensory loss
Cortical lesions - sensory loss, neglect of one side of the body and subtle disorders of sensation
What root value does the ankle jerk reflex correspond to?
S1
What root value does the knee jerk reflex correspond to?
L2, 3, 4
What root value does the biceps jerk reflex correspond to?
C5
What root value does the supinator jerk reflex correspond to?
C6
What root value does the triceps jerk reflex correspond to?
C7
What root value does the abdominals reflex correspond to?
T8-11
corticobulbar tract
component of the pyramidal system.
responsible for transmitting neurones from cerebrum to the cranial nerves.
- control muscles of the face and neck - facial expression
- mastication, swallowing
extrapyramidal system
component of the motor system which do not travel through the pyramids.
- complex movements
- postural control
components of extrapyramidal system
Hint = RPMLT
rubrospinal tract
pontine reticulospinal tract
medullary reticulospinal tract
lateral vestibulospinal tract
tectospinal tract
cranial nerve nuclei that are located in midbrain
CN 1, 2, 3, 4
cranial nerve nuclei that are located in pons
CN 5, 6, 7, 8
cranial nerve nuclei that are located in medulla
CN 5, 7, 8, 9, 10, 11, 12
causes of anosmia (first cranial nerve pathology)
nasal congestion (most common)
anterior fossa tumours
head injury
what structure do the optic nerves enter the cranial cavity through?
optic foramina
Outline the course of the optic nerve
Optic nerve transmitted into the cranial cavity
Forms optic chiasm
Continued as the optic tracts
Fibres of the optic tract project to the visual cortex of the occipital lobe through the lateral geniculate body and third cranial nerve nucleus for pupillary light reflex.
Specific visual field losses can indicate a specific pathology. What does the presence of paracentral scotoma indicate?
Retinal lesion
Specific visual field losses can indicate a specific pathology. What does the presence of monocular field loss indicate?
Optic nerve lesion
Specific visual field losses can indicate a specific pathology. What does the presence of bitemporal hemianopia indicate?
Chiasmal lesion
Specific visual field losses can indicate a specific pathology. What does the presence of homonymous hemianopia indicate?
Optic tract/radiation/cortex/pole lesion (usually due to posterior cerebral artery infraction)
Specific visual field losses can indicate a specific pathology. A lesion in what lobe(s) of the brain may present as a homonymous quadrantanopia indicate?
Temporal/parietal lesion
Name some causes for persistent pupillary dilatation
A third cranial nerve palsy
Antimuscarinic eye drops
Myotonic pupil (no pathological indication - no constriction on light or convergence)
Name some causes of persistent pupillary constriction
- Parasympathomimetic eye drops (used in treatment of glaucoma)
- Horner’s Syndrome
- Argyll Robinson pupil (abnormality seen in neurosyphilis - absent reaction to light but convergence causes constriction)
- Opiate addiction
A palsy of the seventh cranial nerve, cerebellar signs and involvement of the fifth, sixth and eighth cranial nerves indicates a lesion at what anatomical position?
Cerebellopontine angle (most commonly meningioma or acoustic neuroma)
What is the motor function of the trochlear nerve (CN IV)?
Superior oblique muscle
What is the motor function of the abducens nerve (CN VI)?
Lateral rectus muscle
What is the motor function of the oculomotor nerve (CN III)?
Superior, inferior and medial rectus muscles
Sphincter pupilae
Levator palpebrae superioris
The brainstem, cortex and cerebellum coordinate the third, fourth and sixth cranial nerve to ‘conjugate’ eye movements. What is the clinical presentation of a defect in this coordination (called supranuclear palsy)?
Lead to paralysis of conjugate movements of the individual muscles innervated by the third, fourth and sixth cranial nerves
Describe the clinical picture of an infranuclear palsy of the third cranial nerve
Unilateral complete ptosis with ‘down and out’ appearance
Total paralysis leads to a dilated, fixed pupil
Partial paralysis paralysed pupil but still reacted to reactive to light
Describe the clinical picture of an infranuclear palsy of the fourth cranial nerve
Torsional diplopia (two objects at an angle) when attempting to look down
Head is tilted away from the side of the lesion
Describe the clinical picture of an infranuclear palsy of the sixth cranial nerve
The eye cannot be abducted beyond the midline
Eye turns in medially with concurrent diplopia
What is the most common cause of a total and partial third cranial nerve palsy respectively?
Total palsy - berry aneurysm of the posterior communicating artery
Partial palsy - diabetes mellitus
What is often the earliest sign of a fifth cranial nerve lesion?
Diminution of the corneal reflex
What is the clinical presentation of a total fifth cranial nerve palsy?
Unilateral sensory loss on the face, tongue and buccal mucosa with jaw deviation to the side of the lesion
What is the cardinal feature of a supranuclear palsy of the fifth cranial nerve?
Brisk jaw jerk reflex
What is trigeminal neuralgia?
Severe paroxysms of knife-like pain occur in one or more sensory divisions of the trigeminal nerve brought on by a specific trigger
No objective clinical signs
How is trigeminal neuralgia treated?
Anticonvulsant carbamazepine suppresses attacks
Thermocoagulation of the tigeminal ganglion may be necessary
What are the two major branches of the seventh cranial nerve unrelated to facial muscle innervation?
Chorda tympani - providing taste to the anterior two third of the tongue
Nerve to the stapedius - dampening effect on sound
What are the potential features of a facial nerve palsy in addition to the paralysis of facial muscles?
Hyperacusis (undue sensitivity to sounds)
Loss of taste to the anterior two thirds of the tongue
Outline the features of a lower motor neurone lesion of the facial nerve
Ipselateral weakness of the facial muscles
Hyperacusis
Loss of taste of the anterior two thirds of the tongue
What is Bell’s Palsy?
Common, acute isolated unilateral facial nerve palsy probably due to a viral herpes simplex infection causing swelling within the petrous part of the temporal bone
How is a lower motor neurone facial palsy managed?
Protect cornea from ulceration Oral prednisolone (60mg/day for 10 days)
Antivirals used in severe cases
What is the differential diagnosis of paralysed facial muscles?
Bell’s Palsy
Ramsey-Hunt Syndrome
Parotid Tumour
What is Ramsey-Hunt Syndrome?
Herpes zoster (shingles) of the geniculate ganglion causing facial muscles palsy and herpetic vesicles of the external auditory meatus/soft palate
Outline the features of an upper motor neurone lesion of the facial nerve
Weakness of the lower part of the face on the side opposite to the lesion
Wrinkling of the forehead and eye closure are normal
What are the features of an eighth cranial nerve palsy?
Cochlear nerve branch - sensorineural deafness and tinnitus
Vestibular nerve branch - vertigo +/- nausea/vomiting
List some causes of eighth nerve palsy
Brainstem (tumour, mutiple sclerosis)
Cerebellopontine angle (acoustic neuroma)
Petrous temporal bone (trauma, middle ear infection)
What is nystagmus?
Rhythmic oscillation of the eyes
What are the two types of nystagmus?
Pendular - no rapid phase (due to longstanding visual impairment)
Jerk - rapid and slow phases (two subtypes: horizontal or vertical)
The lower four cranial nerves lie in the medulla (the “bulb”) are usually affected together. Outline the features of a lower motor neurone type palsy of the bulbar cranial nerves (bulbar palsy)
Dysarthria (slow speech)
Dysphagia
Nasal regurgitation
Wasting and fasciculation of the tongue
What are the most common causes of bulbar palsy?
Motor neurone disease
Syringobulbia (fluid-filled cavity in the brainstem)
Outline the features of an upper motor neurone type palsy of the bulbar cranial nerves (pseudobulbar palsy)
Weakness of the muscles of speech and swallowing with small, spastic tongue (no wasting or fasciculation)
What are the most common causes of pseudobulbar palsy?
Motor neurone disease
Multiple sclerosis
What is normal CSF pressure?
80-120 mmH2O
What is the purpose of nerve conduction studies?
Differentiates between axonal and demyelination neuropathy
What are some known complications of lumbar punctures?
Post-procedure headache, infection, herniation (coning)
What are the cardinal investigations of suspected muscle disease? (4)
Serum creatine kinase and aldose EMG Muscle biopsy (histology and immunohistochemical staining)
What area of the brain is chiefly responsible for states of arousal?
Reticular formation (extending from the brainstem to the thalamus)
What is coma?
A state of unconsciousness from which the patient cannot be roused
What is a stuporous state?
When a patient is sleepy but can be roused with vigorous stimulation
A patient unresponsive to anything except pain is broadly corresponsive to what GCS level?
8
What must coma be differentiated from?
Persistent vegetative state
Brain death
Locked-in syndrome
What is a persistent vegetative state?
A state of wakefulness in which sleep-wake cycle persists but without detectable awareness
What is the cardinal sign of brain death?
Bilaterally fixed and dilated pupils
What are dysconjugate eyes a sign of?
Brain stem lesion
Conjugate lateral deviation of the eyes indicates what two potential pathologies?
Ipselateral cerebral haemorrhage/infarction
Contralateral pontine lesion
What is brain death?
Irreversible loss of the capacity for consciousness, combined with the irreversible loss of the capacity to breathe
What are the three main criteria of the diagnosis of brain death?
- Irremediable structural brain damage
- Absent motor responses to any stimulus
- Absent brainstem function (lack of pupillary, corneal, gag, cough, doll’s head or caloric reflexes, lack of spontaneous breathing)
What is the definition of a stroke?
Rapid onset of neurological deficit lasting greater than 24-hours, which is the result of a vascular origin.
What is the definition of stroke in evolution?
When symptoms and signs are getting worse (usually within 24-hours of onset)
What is the definition of a minor stroke?
When the patient recovers without significant neurological deficit, usually within one week
What is the definition of a transient ischaemic attack?
Transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction.
Arterial thrombosis causing stroke can arise from what locations?
Atheromatous plaques
Cardiac mural thrombi (post-MI)
Left atrium (due to atrial fibrillation)
What is the differential diagnosis of stroke?
Intracranial venous thrombosis
Multiple sclerosis
Space-occupying lesion e.g. tumour/abscess
In young adults, 20% of are caused by carotid/vertebral artery dissection. What clinical picture might be suggestive of this pathophysiology?
Recent neck pain, trauma or neck manipulation
What are the major risk factors for thromboembolic stroke?
Hypertension, diabetes mellitus, cigarette smoking, hyperlipidaemia, obesity, excessive alcohol consumption
What are the differential diagnoses for transient ischaemic attack?
Demyelination, tumour
How is the risk of stroke measured following a confirmed TIA?
ABCD2 risk
Hemiplegia is often caused by infarction of what area of the brain during a cerebral haemorrhage stroke?
Infarction of the internal capsule
What is the internal capsule?
Narrow zone of motor and sensory fibres that converges on the brainstem from the cerebral cortex
Brainstem infarction can manifest in a number of different clinical presentations. Name a few. (4)
Lateral medullary syndrome
Coma
Locked-in syndrome
Pseudobulbar palsy
What is lateral medullary syndrome?
Most common of the brainstem vascular syndromes caused by occlusion of the posteiror inferior cerebellar artery
Presents as sudden vomiting, vertigo, facial numbness, Horner’s syndrome, diminished gag reflex
Coma as a result of stroke is caused by infarction of what site in the brain?
Reticular activating syndrome
Upper brainstem stroke causes what pathology?
Locked-in syndrome
Lower brainstem stroke causes what pathology?
Pseudobulbar palsy
What is multi-infarct dementia?
Also called vascular dementia
Multiple small cortical infarcts resulting in generalised intellectual loss with step-wise progression
Clinical picture of dementia, pseudobulbar palsy and Parkinsonian ‘shuffling’ gait
What is the indicated acute treatment of stroke?
Aspirin (300mg ASAP)
Thrombolysis (IV tPA) given within 4.5hrs in acute ischaemic stroke
What secondary interventions are put in place following acute stroke?
Hypertension management
Carotid endarterectomy (in the case of stenosed carotid artery to prevent recurrence of stroke)
Address other modifiable risk factors including smoking, obesity etc.
What are the major risk factors for intracerebral haemorrhage?
Hypertension, excess alcohol consumption, increasing age and smoking
What is the presentation of intracerebral haemorrhage?
Sudden loss of consciousness and stroke often accompanied by severe headache
What is a subarachnoid haemorrhage?
Refers to spontaneous arterial bleeding into the subarachnoid space
What is the radiological appearance of a subarachnoid haemorrhage?
Hyperdense appearance typically around the branching points of arteries of the Circle of Willis
What are the most common aetiologies of subarachnoid haemorrhage?
Rupture of saccular ‘berry aneurysms’
Congenital arteriovenous malformation
What are the symptoms of a berry aneurysm before it ruptures?
Often asymptomatic before they rupture
Any symptoms are due to mass effect, most commonly a painful third cranial nerve palsy
What are the symptoms of a berry aneurysm when it ruptures?
Sudden onset of severe headache (often occipital), accompanied by nausea and vomiting
Potential loss of consciousness and meningeal irritation (neck stiffness and positive Kernig’s sign)
Lumbar punctures must be delayed until at least 12 hours after onset of symptoms in order to confirm diagnosis. Why is this?
To allow sufficient time for haemoglobin to degrade into oxyhaemoglobin and bilirubin (detectable for up to two weeks following SAH)
How is subarachnoid haemorrhage immediately managed?
Best rest and supportive measures with control of hypertension and IV nimodipine (CCB) to reduced cerebral artery spasm.
Discussion with neurosurgeon for obliteration of aneurysm to prevent re-bleeding
What is a subdural haematoma?
Accumulation of blood in the subdural space following a venous bleed.