Neurology

Question 1

Label the constituent portions of the cerebral cortex. (Frontal, parietal, temporal, occipital)

Answer 1

Frontal: associated with executive function, motor cortex, and on the dominant hemisphere,
speech/language (Broca’s area).
Parietal: in which the somatosensory cortex lies, is also responsible for numerical calculation. The
non-dominant parietal lobe is responsible for spatial awareness and positioning.
Temporal: involved in olfaction, memory, emotional function, and auditory capabilities. On the
dominant side, Wernicke’s area is located on the superior
Occipital: primarily involved in visual function.

Question 2

What syndrome would arise from a brainstem lesion?

Answer 2

Bulbar palsy: Lower motor neuron weakness of muscles supplied by the cranial nerves with cell bodies in the medulla, i.e. the ‘bulb’ - CN IX, X & XII (signs assoiated with these Cranial nerves)

Question 3

What would happen in a patient with cerebral hemisphere lesions?

Answer 3

Can lead to impairments of higher function although the type of function impaired depends on where.
Frontal lesions: Intellectual impairment, personality change, urinary incontinenece and monopariesis/hemiparesis. Broca’s aphasia (if left frontal area)
Left temporo-paritetal (dominant hemisphere): Agraphia (inability to write),, alexia (inability to understand written words), acalculia (inability to do simple maths), wernicke’s aphasia, contralateral sensory neglect
Right temporoparietal: failure of facial recognition, contralateral sensory neglect
Occipital: visual field defects, visuospatial defects

Question 4

What would happen in a patient with cerebellar lesions?

Answer 4

Damage will cause nystagmus, dysarthria (unclear speech), intention tremor and ataxia. There is no
weakness or sensory loss. Lesions cause ipsilateral loss of function. Interruption of proprioceptive
centres will cause sensory ataxia and positive Romberg’s sign. (DANISH – dysdiadochokinesis, ataxia,
nystagmus, intention tremor, slurred speech (scanning dysarthria – HI PO POT A MUS), hypotonia.)

Question 5

What structures make up the basal?

What is the overall function of the basal ganglia?

Answer 5

The basal ganglia is also known as the extra-pyramidal system:
-Corpus stratum: caudate nucleus, globus pallidum and putamen
-Subthalamic nucleus
-Substantia nigra
-Parts of the thalamus
The overall function of the basal ganglia is to modulate cortical motor activity

Question 6

What would happen in a patient with basal ganglia lesions?

Answer 6

Bradykinesia (can progress to akinesia), muscle ridigity, involuntary movements: tremor, dystonia (spasms/abnormal muscle contractions), athetosis (writhing involuntary movement of hands, face or tongue, chorea (jerky involuntary movements), hemiballismus (violent involuntary movement, restricted to proximal muscles of just one arm)

Question 7

What is homonymous hemianapia?

Where would the legion be if a patient has homonymous hemianopia?

Answer 7

Homonymous hemianopa is hemianopic visual field loss on the same side of both eyes (insert picture)
Contralateral optic tract lesion
(insert picture - page 151 one salt too sweet or wikipedia)

Question 8

What is bitemporal hemianopia?

Where would the legion be if a patient has it?

Answer 8

where vision is missing in the outer half of both the right and left visual field
Optic chiasm lesion

Question 9

Insert pic from pg 151 one salt too sweet

What numbers correlate to what visual disturbances?

Answer 9

Match up with the other picture

Question 10

Describe the clinical difference between upper and lower motor neuron facial weakness.
Give an example of an UMN and LMN causing facial weakness

Answer 10

The forehead is spared in unilateral UMN lesion to CN VII.
In the face, LMN lesions cause ipsilateral facial weakness of all muscle of facial expression. An example is facial nerve (CN VII) palsy (also known as Bell’s palsy)
UMN lesions cause contralateral facial weakness, but spare frontalis, as this receives supranuclear innervation from both hemispheres - furrowing of the brow, eye closing and blinking are preserved. An example of an UMN lesion is a stroke

Question 11

Draw the motor pathway, labelling its main constituents, that is, the upper motor neuron, lower motor neuron, neuromuscular junction and muscle, with respect to structures in the central and peripheral nervous system

Answer 11

look back at FBN medsoc teaching on the motor pathway
Insert picture
http://www.bioon.com/bioline/neurosci/course/basmot.html

Question 12

Describe the clinical difference between upper and lower motor limb weakness

Answer 12

LMN signs: Weakness, Wasting, Fasciculation, Hypotonia, Hyporeflexia
UMN signs: Weakness (characteristically flexor weakness in upper limb, extensor weakness in lower limb), no wasting, Hypertonia, spasticity, hyperreflexia, loss of fine motor movements, pronator drift, extensor plantar response, clonus

Question 13

What are the ddx for LMN lesions?

Answer 13

Ventral horn pathology - (Motor Neuron Disease, post polio)
Peripheral nerve pathology
Neuromuscular junction patholgy (Myasthenia Gravis)
muscular patholgy

Question 14

What are the ddx for UMN lesions?

Answer 14

Vascular: stroke
Inflammatory: Multiple sclerosis, motor neuron disease
Neoplastic: tumour
Degenerative: Parkinson's
Infective: Post-meningitis
Extras: Drugs

Question 15

What clinical syndrome/findings would arise from S1 root lesion?
Typical history?

Answer 15

Sensory loss: Posterior calf, lateral border of foot
Reflex loss: Ankle
Motor loss: Plantar flexion
History: Dramatic onset during twisting, lifting or bending

Question 16

What clinical syndrome/findings would arise from C5 root lesion?

Answer 16

Sensory loss: Lateral arm
Reflex loss: Biceps
Motor loss: Shoulder Abduction and Elbow Flexion

Question 17

What clinical syndrome/findings would arise from median nerve compression at the carpal tunnel?

Answer 17

Sensory loss: (paraesthesia - abmormal sensation e.g. tingling, numbness, burning ect.), Palmar aspect of first 3.5 digits (picture)
Insert picture of where median nerve is
Motor loss: Wasting of Pollicus Brevis (picture of where that is)

Question 18

What clinical syndrome/findings would arise from ulnar nerve palsy?

Answer 18

Sensory loss; Medial 1.5 digits (pink and half of ring finger)
Motor loss: Wasting of hypothenar muscles (all 3), interossei and medial 2 lumbricals (picture of where they are)

Question 19

What clinical syndrome/findings would arise from radial nerve palsy?

Answer 19

Sensory loss: Dorsum of hand (picture)

Motor loss: Brachioradialis and finger extensors

Question 20

Define stroke with reference to time course

Answer 20

Syndrome of rapid onset of cerebral deficit lasting >24hrs or leading to death, with no apparent cause other than a vascular one
Transient Ischaemic Attack = Sudden focal deficit lasting from seconds to 24hrs with complete
recovery.
• Amaurosis Fugax = Sudden transient loss of vision in one eye. Found prior to carotid system TIA.

Question 21

Define Transcient Ischaemic attack (TIA) with reference to time course

Answer 21

An acute, focal neurological deficit of cerebrovascular origin that persists <1 hour, without signs of cerebral infarction on MRI scanning. Complete recovery

Question 22

Define amaurosis fugax with reference to time course

Answer 22

Sudden transient (short term) loss of vision in one eye
Often occur with TIAs and be the first clinical evidence of internal carotid artery stenosis. Can also occur due to ocular disease or migraine

Question 23

List the modifiable (reversible) risk factors leading to the development of ischaemic stroke

Answer 23

Hypertension, hypercholesterolemia, diabetes, smoking, alcohol, poor diet, low exercise, obesity, use of oestrogen-containing oral contraceptives

Question 24

List the non-modifiable (irreversible) risk factors leading to the development of ischaemic stroke

Answer 24

Age, family history, hyper-coagulable states, atrial fibrillation

Less common risk factors: endocarditis, migraine, polycythaemia, APL syndrome, vasculitis, SLE or amyloidosis

Question 25

What are the risk factors for haemorrhagic stroke?

Answer 25

Family history, uncontrolled hypertension, vascular abnormalities (aneurysms, arteriovenous malformation,, Hereditary haemorrhagic telangiectasia), coagulopathies/anticoagulant therapy, heavy recent alcohol intake

Question 26

What are the two different types of stroke? (% if each one)

What are the sub-types

Answer 26

1. infarction (85%)
   - Arterial embolus from a distant site
   - Arterial thrombosis in atheromatous carotid, vertebral or basilar artery
2. Haemorragic (15%)
   - Sub arachnoid haemorrhage 10%
   - Intra-cerebral haemorrhage 5%

Question 27

What are the different types of cerebral ischaemia?

Answer 27

Regional infarction:
-Thrombus/embolus in large vessels, usually affects cortical areas
Lacunar infarctions:
-Microinfarcts caused by small vessels disease: arteriolosclerosis, usually affecting sub-cortical areas e.g. basal ganglia - can be asymptomatic, eventually leading to vascular pseudo-parkinsonism or vascular dementia
Global ischaemia:
- Infarcts at arterial boundary zones due to a global reduction in blood flow due to severe hypotension (aka watershed infarction)
-If severe, can cause cortical laminar necrosis, where there is death of the majority of neurons 24 hours after the insult, with the pt remaining in a vegetative state (part of the ‘post arrest syndrome’)

Question 28

In any area of cerebral ischaemic damage it is considered that there are 3 zones. What are the 3 zones?

Answer 28

Infarct core: tissue almost certainly dies
Oligaemic periphery: tissue that will survive ,due to collateral supply
Ischaemic penumbra: tissue in between, can either outcome
(insert picture)

Question 29

What are the clinical features of ischaemic stroke?

Answer 29

-Contralateral limb weakness/hemiplegia
(At first flaccid, but over a period of time reflexes return and become exaggerated, with extensor plantars)
(Weakness is maximal at first and recovery occurs gradually over weeks to months)
-Facial weakness
-Higher dysfunction
-Visual disturbances
-Epileptic fit (rare)

Question 30

What are examples of higher dysfunction that may occur due to a stroke?

Answer 30

Expressive aphasia - inability to express language despite intact comprehension
Receptive aphasia - inability to understand commands and the world around them. May have fluent but meaningless speech
Apraxia - Difficulty in performing tasks despite intact motor function
Asterognosis - Inability to identify objects in both hands by touch alone despite intact sensation
Agnosia - Inability to recognise objects, persons, sounds, shapes or smells despite the specific sense being intact and no memory loss
Inattention - inability to attend to stimuli despite intact senses

Question 31

Describe the pathological causes and consequences of ischaemic stroke

Answer 31

Most commonly caused by local arterial disease (occlusion and stenosis). Occlusion may occur
following thrombosis on an atheromatous plaque in either the internal carotid/verterbral artery or
intracerebral artery. Emboli are commonly derived from the heart, as in AF, infective endocarditis
and mural thrombi/ventricular aneurysm (don’t forget paradoxical embolus!). Emboli may also come
away from ulcerated atheroma in the carotid artery. Stenosis (atheromatous) on its own is not
usually a cause of infarction but a small drop in BP can cause watershed infarct/infarct in the
territory of the stenotic artery.
Up to 24 hours there is little gross appearance of infarction. After 24 hours, there is some swelling
and blurring of the junction between white and grey – accompanied by a microscopic picture of
necrosis. After a few days, a line of demarcation is seen between necrotic and viable tissue – the
infarct begins to “organise”, macrophages infiltrate, oedema lessens, and capillaries begin to sprout.
Weeks later, demolition of the necrotic tissue has occurred, the scarred area shrinks and the
ventricle enlarges on the same side

Question 32

Describe the pathological causes and consequences of haemorragic stroke

Answer 32

Most commonly occurs in hypertensives. Past middle age, microaneurysms develop in patients with
hypertension, and rupture of one of these is the cause of intracerebral haemorrhage. The onset is
with sudden headache, then ICP develops, and death often follows. Haematoma forms, most
commonly in MCA branches to the BG and internal capsule, but also in the pons and cerebellum.
When bleeding is limited, patients may survive with limited paralysis. The final outcome is
development of a cyst, walled by glia, containing yellow-brown fluid.

Question 33

Describe how atrial fibrillation gives rise to stroke

Answer 33

Blood becomes turbulent and relatively static in atria contracting incoordinantly. This increases risk
of thrombosis in the heart. Thromboemboli are responsible for 80% of TIAs and 70% of strokes.

Question 34

Describe the clinical presentation of a subarachnoid stroke

Answer 34

‘Thunderclap’ headache
- Develops over seconds, devastating in intensity, often occipital
-Often comes on during times of transient hypertension, such as physical activity or sex
Vomiting - comes on after headache
Photophobia
Increasing drowsiness/coma
Focal signs may point to the location of the lesion
-However may reflect raised ICP (false localizing sign) or cerebral vasospasm due to the irritant effect of blood

Question 35

What would be found on clinical examination of a pt who had suffered a subarachnoid haemorrage?

Answer 35

Neck stiffness
Positive Kernig’s sign (Pain on extension of a previously flexed knee and hip 90 degrees) - takes 6 hours to develop
Papilloedema: may be present, along with retinal haemorrhages
SAH may mimic an MI on the ECG due to the adrenaline release.
One of three brudzinski’s signs is flexion ofthe elbow in response to pressure to the cheek; another is flexion of the hip in response to flexion of the neck, and the last is abduction and flexion of the hip in response to pubic symphysis pressure

Question 36

Describe the clinical features of meningism

Answer 36

Neck stiffness, photophobia, and headache = meningism = meningeal irritation

Question 37

What are the two main vascular abnormalities which may predispose a patient to developing a subarachnoid haemorrage?

Answer 37

Berry aneurysm (70%)
Arteriovenous malformations (AVM - 10%)

Question 38

What is a berry aneurysm? Describe its pathophysiology

Answer 38

-Develops in the circle of Willis and adjacent arteries
-Locations: Anterior communicating artery (most common), Posterior communicating artery (at bifurcation of ICA) and middle cerebral artery (at bifurcation)
-More common in those with polycystic kidney disease
Congenital weakness in the elastic tissues lining arteries. These thin walled aneurysms develop at sits of deficiency in arteries
(Insert picture)

Question 39

What are arteriovenous malformations? Describe their pathophysiology

Answer 39

• Congential collection of abnormal arteries/veins without intervening capillaries, and often wound up into bundles of vessels
• Due to the abnormal blood pressure distribution, these structures are at risk of rupture, leading to haemorrhage
• Have a tendency to rebleed if symptomatic once
• Can cause epilepsy, often focal

Question 40

List the potential complications of a subarachnoid haemorrage

Answer 40

-Death (30% of patients will die immediately)
-Rebleed
(Aneurysms - If vasospasm is sufficient, a clot can form but it only holds for 3-4 days before rebleeding)
(AVMs - generally rebleed within a few years rather than days)
-Hydrocephalus (build up of fluid in briain, increases pressure - in this case due to fibrosis in the CSF pathways)
-Cerebral vasospasm (Can be severe, leading to delayed ischaemic damage)

Question 41

Define subdural haematoma

Answer 41

Collection of blood in the subdural space following rupture of a vein, usually following a head injury, although can occur spontaneously

Question 42

What predisposing factors makes a patient vulnerable to developing a subdural haemorrage?

Answer 42

Common in the elderly and alcoholics (cerebral atrophy) and occurs with anticoagulants. Often
extensive due to loose attachment of the dura and arachnoid membranes, usually occurs with
rupture of small bridging veins, at the point where they enter the dura. In at risk groups, bridging
veins may become stretched and more susceptible to damage

Question 43

Describe the clinical presentation of a chronic subdural haemorrage

Answer 43

May be long prodrome following trivial trauma. Interval between trauma and sign and symptoms may be weeks.
Headache, drowsiness and confusion and common, and may fluctuate. Focal deficits and epilepsy
develop. Stupor, coma and coning may follow.
Pathology: a layer of fluid and partially clotted blood forms between the dura and arachnoid, which
both thicken reactively. There is pressure atrophy of the brain.

Question 44

Define meningitis

Answer 44

Inflammation of the leptomeninges

I.e. the arachnoid and pia mater, and underlying CSF

Question 45

What are the common bacterial and viral organisms which cause meningitis in adult life?

Answer 45

Outside of the neonatal period, 70% of acute bacterial meningitis cases are caused by:
-Neisseria menigitidis
-Streptococcus pneumonia
The other 30% are a wide variety of causes: e.g. listeria monocytogenes, haemophilus influenza, staph aureus & TB

Viral causes:

• Enteroviruses (coxsackie A/B, echoviruses)
• HSV
• VZV

Question 46

Outline the clinical presentation of bacterial meningitis

Answer 46

Meningitic syndrome triad: Headache, Neck stiffness, Fever
Also commonly be a high fever with rigors, photophobia, vomiting and intense malaise coming on over hours.
Confusion and seizures can develop in more serious cases

Question 47

Describe the appearance of the typical rash of meningococcal septicaemia

Answer 47

The rash in meningococcal septicaemia is “petechial”, blotchy, and non-blanching.
It may be found anywhere on the body

Question 48

Which is more dangerous bacterial or viral meningitis?

Answer 48

Bacterial
Viral meningitis is almost always a benign, self limiting condition, which lasts 4-10 days - headache may last for some moths but no serious sequalae

Question 49

What complications may arise from meningitis?

Answer 49

Venous sinus thrombosis, cerebral oedema, hydrocephalus, papilloedema, chronic headache, and
septicaemic shock may arise from meningitis.
Others include hearing loss, seizures, cortical blindness, peripheral infection & gangrene, and death.