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Phase 2a Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

features of 3rd nerve palsy

A

Parasympathetic fibres on outside of nerve
Over apex of petrous part of temporal bone
Fixed dilated pupil

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2
Q

5 key landmarks on the base of the skull/ posterior fossa

A

Petrous apex/cavernous sinus/ orbital apex
Internal acoustic meatus
Jugular foramen

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3
Q

foramina involved in obstructive hydrocephalus

A

Foramina of Magendie and Lushka

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4
Q

5 brainstem-associated neural structures

A

Cranial nerves III-XII
Descending motor tracts (pyramidal tracts)
Ascending sensory tracts (Lemnisci)
Reticular activation
Cerebellar peduncles

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5
Q

3 structures involved in the ascending sensory system

A

Thalamus
Posterior columns
Lateral spinothalamic tract

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6
Q

3 structures involved in the descending motor system

A

Internal capsule
Pyramidal decussation
Corticospinal tract

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7
Q

3 nerve fibre types in motor nerves

A

Somatic
Branchial (motor only)
Autonomic

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8
Q

3 nerve fibre types in sensory nerves

A

Somatic
Autonomic
Special (sensory only)

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9
Q

Autonomic nerve features

A

Arise in the most evolutionary primitive parts of the brain
No conscious control
Smooth and cardiac muscle
Glands

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10
Q

What is a dermatome

A

area of skin supplied by a single spinal nerve

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11
Q

what is a myotome

A

a volume of muscle supplied by a single spinal nerve

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12
Q

Course and features of corticospinal tract

A

Starts in the cortex
Ends in the spinal cord
A well-defined bundle of white matter
Motor
From the precentral gyrus
Through internal capsule
Crura cerebri
85% decussates medulla – lateral tract
15% same side – anterior tract

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13
Q

Why use epidural anaethetic

A

The spinal cord finishes at L1
The corda equina continues through the lumbar vertebra
The cell bodies for the sensory neurones are in the dorsal root ganglia
Cell bodies have a higher surface area and take up anaesthetic better than axons
Epidural anaesthetic gives a greater sensory block than motor block

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14
Q

Branches off the aortic arch

A

Brachiocephalic trunk – divides into right common carotid and right subclavian arteries
Left common carotid artery
Left subclavian artery
Left vertebral artery

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15
Q

features of Common carotid arteries

A

Right CCA arises from the brachiocephalic artery
Left CCA arises from the aortic arch
They have no branches
The CCAs bifurcate at approx. C3-C4

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16
Q
A
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17
Q

.

A

No narrowings/ dilatations/ branches
Anterior and medial to internal jugular vein
Lies posterior and lateral to ECA at origin
Ascends behind and then medial to ECA
Rare carotid-basilar anastomoses

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18
Q

course of the petrous ICA

A

Penetrates temporal bone and runs horizontally (anteromedially) in the carotid canal
Small branch to middle/ inner ear (caroticotympanic artery)
Small potential connection with ECA – vidian artery

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19
Q
A
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20
Q

course of the supraclinoid ICA

A

Ophthalmic artery is usually intradural and passes into optic canal
Superior hypophyseal arteries/ trunk supply pituitary gland, stalk, hypothalamus and optic chiasm
Posterior communicating artery runs backwards above CN3 to connect with the PCA
Anterior choroidal artery supplies choroid plexus, optic tract, cerebral peduncle, internal capsule and medial temporal lobe

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21
Q

4 types of inter-cranial haemorrhage

A

Extradural haemorrhage
Subdural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

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22
Q

3 layers of the meninges

A

Dura, usually firmly adherent to the inside of the skull
Arachnoid, more adherent to the brain
Pia, on the surface of the brain and cannot be separated from the brain

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23
Q

blood vessels of the meninges

A

Meningeal vessels are in the extradural space
Bridging veins cross the subdural space
The circle of willis lies in the subarachnoid space
There are no vessels deep to the pia, the pia forms part of the blood brain barrier

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24
Q

features of extradural haemorrhage

A

Traumatic
Fractured skull
Bleeding from middle meningeal artery
Lucid period
Rapid rise in inter-cranial pressure (ICP)
Coning and death if not treated

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25
Q

features of subdural haemorrhage

A

Bleeding from bridging veins
Commonest where the patient has a small brain (alcoholics, dementia)
Occurs in shaken babies
Bridging veins bleed, low pressure so soon stops
Days/ weeks later the haematoma starts to autolyse
Massive increase in oncotic and osmotic pressure sucks water into the haematoma
Gradual rise in ICP over many weeks

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26
Q

features of subarachnoid haemorrhage

A

Rupture of the arteries forming the circle of Willis
Often because of berry aneurysms
Sudden onset severe headache photophobia and reduced consciousness
Thunderclap headache
Rapidly fatal, the commonest source of organs for transplant since seat belts were made compulsory

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27
Q

features of embolic stroke

A

Death of cell bodies in the cortex
Small well-defined territory of loss of motor and sensory function
No recovery

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28
Q

features of haemorrhagic stroke

A

Compression of the internal capsule with no death of cells
Large territory of loss of motor and sensory function
Possibility of complete recovery

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29
Q

cerebrovascular disease

A

Cerebrovascular diseases are conditions caused by problems that affect the blood supply to the brain.

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30
Q

4 most common types of cerebrovascular disease

A

Stroke
Transient ischaemic attack
Subarachnoid haemorrhage
Vascular dementia

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31
Q

5 causes of stroke

A

Small vessel occlusion/cerebral microangiopathy or thrombosis in situ
Cardiac emboli
Atherothromboembolism
CNS bleeds e.g. trauma, aneurysm rupture
Subarachnoid haemorrhage, venous sinus thrombosis, thrombophilia

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32
Q

5 modifiable risk factors for stroke

A

High blood pressure
Smoking
Diabetes mellitus, heart disease, peripheral vascular disease

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33
Q

5 conditions which can cause stroke

A

hypertension, cardiac source of emboli, carotid artery stenosis, vasculitis, hyper viscosity.

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34
Q

pathology of ischaemic stroke

A

sustained occlusion of a cerebral artery leads to ischaemic necrosis of the territory of the brain supplied by the affected artery.

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35
Q

pathology of haemorrhagic stroke

A

Most cases related to hypertension are due to ruptured Charcot-Bouchard microaneurysms
A haematoma forms which destroys the brain structure and causes a sudden rise in intracranial pressure

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36
Q

when are stroke symptoms worst

A

Worst at onset.

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37
Q

3 pointers to haemorrhagic stroke

A

meningism, severe headache, coma

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38
Q

4 pointers to ischaemic stroke

A

carotid bruit, AF, past TIA, IHD

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39
Q

clinical manifestations for cerebral infarcts

A

Depending on site there may be contralateral sensory loss or hemiplegia – initially flaccid (floppy limb, falls like a dead weight when lifted)
Becoming spastic (UMN)
Dysphasia
Contralateral homonymous hemianopia, visuo-spatial deficit

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40
Q

clinical manifestations for brainstem infarcts

A

Varied: include quadriplegia, disturbances of gaze and vision, locked-in syndrome (aware, but unable to respond)

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41
Q

clinical manifestations of lacunar infarcts

A

Five syndromes: ataxic hemiparesis, pure motor, pure sensory, sensorimotor, and dysarthria/clumsy hand.

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42
Q

locations of lacunar infarcts

A

Basal ganglia, internal capsule, thalamus, and pons.

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43
Q

differential diagnosis for stroke

A

Head injury
Hypo/hyperglycaemia
Subdural haemorrhage
Intracranial tumours, hemiplegic migraine, CNS lymphoma, Wernicke’s encephalopathy

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44
Q

investigations for stroke

A

FAST: facial asymmetry, arm/leg weakness, speech difficulty, time to call 999
Imaging: CT/ MRI to check for haematoma
ECG: to check for atrial fibrillation
CXR: left ventricular hypertrophy
Carotid doppler ultrasound: to look for stenosis of the carotid

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45
Q

management of ischaemic stroke

A

Thrombolysis- IV altepase
Aspirin for 2 wks then clopidogrel
rehabilitation- physio,OT
stop smoking/alcohol, exercise

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46
Q

Management of haemorrhagic stroke

A

Control BP- beta blocker/ ARB
Beriplex if warfarin related
Surgery- Clot evation
Rehabilitation- physio, OT
Stop smoking/alcohol, exercise

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47
Q

Acute management of stroke

A

Protect the airway: this avoids hypoxia/aspiration
Maintain homeostasis: blood glucose, blood pressure
Screen swallow: ‘nil by mouth’ until this is done
CT/MRI within 1 hour: essential if thrombolysis considered, high risk of haemorrhage
Antiplatelet agents: once haemorrhagic stroke excluded, give aspirin 300mg
Thrombolysis (IV alteplase): consider as soon as haemorrhage has been excluded
Thrombectomy

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48
Q

primary prevention of stroke

A

Control risk factors:
Hypertension
Diabetes mellitus, raised lipids
Cardiac disease
Help to quit smoking
Use lifelong anticoagulant in AF and prosthetic heart valves

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49
Q

secondary prevention for stroke

A

Control risk factors: there is considerable advantage from lowering blood pressure and cholesterol
Antiplatelet agents after stroke
Anticoagulation after stroke from AF

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50
Q

Transient ischaemic attack

A

An ischaemic (usually embolic) neurological event with symptoms lasting <24h (often much shorter).

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51
Q

causes of TIA

A

Atherothromboembolism from the carotid is the chief cause for bruits.
Cardioembolism: mural thrombus post-MI or in AF, valve disease, prosthetic valve
Hyperviscosity: e.g. polycythaemia, sickle-cell anaemia, myeloma
Vasculitis: a rare, non-embolic cause of TIA symptoms

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52
Q

Which score is used to assess TIA risk

A

ABCD2 score

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53
Q

points to the ABCD2 score

A

A – age: 60 years of age or more (1 point)
B – BP 140/90mmHg or greater (1 point)
C – clinical features – unilateral weakness 2 points, speech disturbance without weakness 1 point
D- duration (60 minutes + (2 points), 10-59 minutes (1 point))
D- diabetes (1 point)

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54
Q

What classifies as High risk for TIA

A

ABCD2 score of 4 or more
Atrial fibrillation
More than one TIA in one week
TIA whilst on an anticoagulant

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55
Q

What is amaurosis fugax

A

occurs when the retinal artery is occluded, causing unilateral progressive vision loss ‘like a curtain descending’.

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56
Q

clinical manifestations of TIA

A

Specific to the arterial territory involved.
Global events e.g. syncope, dizziness, are not typical of TIAs
Attacks may be single or many;
Multiple highly stereotyped attacks suggest a critical intracranial stenosis

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57
Q

5 differential diagnoses for TIA

A

Hypoglycaemia
Migraine aura
Focal epilepsy
Hyperventilation
Retinal bleeds

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58
Q

1st line investigations for TIA

A

Bloods: FBC (look for polycythaemia), glucose, ESR (raised in vasculitis), U&Es, cholesterol, INR (if on warfarin), ECG, lipid profile, prothrombin time

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59
Q

Gold standard investigations for TIA

A

Symptoms 10-15mins, <24 hours + no infarction

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60
Q

Controlling CV risk factors for TIA

A

Optimise BP (aim for <140/85mmHg)
Hyperlipidaemia
Diabetes mellitus
Help to stop smokin

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61
Q

Management for TIA

A

Control CV risk factors
Antiplatelet drugs
Anticoagulation indications: cardiac source of emboli
Carotid endarterectomy: surgery to remove a build-up of plaque in the carotid artery

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62
Q

Antiplatelet drugs for TIA

A

As with stroke, give aspirin 300mg OD for 2 weeks, then switch to Clopidogrel 75mg.

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63
Q

Subarachnoid haemorrhage

A

A spontaneous, non-traumatic bleed into the subarachnoid space.

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64
Q

Aetiology of subarachnoid haemorrhage

A

Most commonly due to rupture of a berry aneurysm
It has been hypothesised that a congenital defect in the tunica media of the cerebral vessels leads to aneurysm formation later in life due to atherosclerosis and hypertension.
Arterio-venous malformations
Encephalitis, vasculitis, tumour invading blood vessels, idiopathic.

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65
Q

Pathology of Subarachnoid haemorrhage

A

Most berry aneurysms arise at the site of arterial bifurcation at the base of the brain
Rupture of the aneurysm usually results in extensive bleeding through the subarachnoid space. The haemorrhage may extend into the brain tissue, as well as the ventricular system.

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66
Q

5 risk factors for Sub arachnoid haemorrhage

A

Previous aneurysmal SAH
Smoking/ alcohol misuse
Raised BP
Bleeding disorders
Polycystic kidneys, aortic coarctation and Ehlers-Danlos syndrome are all associated with berry aneurysms.

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67
Q

5 symptoms of Subarachnoid haemorrhage

A

Sudden-onset excruciating headache – like a thunderclap
Vomiting
Collapse
Seizures
Coma/drowsiness – may last for days

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68
Q

Signs of Subarchnoid haemorrhage

A

Neck stiffness
Kernig’s sign (severe stiffness of the hamstrings – can’t straighten leg when hip is flexed)
Retinal, sub-hyaloid and vitreous bleeds

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69
Q

complications of subarachnoid haemorrhage

A

re-bleeding from the aneurysm, CSF malabsorption problems, and arterial vasospasm

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70
Q

differential diagnoses for Subarachnoid haemorrhage

A

Meningitis
Migraine
Intracerebral bleed
Cortical vein thrombosis
Benign thunderclap headache (triggered by Valsalva manoeuvre e.g. cough, coitus)

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71
Q

investigations for subarachnoid haemorrhage

A

Macroscopy: blood is present within the subarachnoid space, often with abundant clots around the circle of Willis at the base of the brain.
Urgent CT: detects 95% of subarachnoid haemorrhages

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72
Q

Management of subarachnoid haemorrhage

A

Re-examine CNS often: chart BP, pupils and GCS. Repeat CT if deteriorating
Maintain cerebral perfusion by keeping well hydrated
Nimodipine is a calcium antagonist that reduces vasospasm and consequent morbidity from cerebral ischaemia
Mannitol – decreases ICP
Surgery: endovascular coiling vs surgical clipping (requiring craniotomy) – decision depends on accessibility and size of aneurysm

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73
Q

complications of subarachnoid haemorrhage

A

Re-bleeding – commonest cause of death
Cerebral ischaemia due to vasospasm may cause a permanent CNS deficit
Hydrocephalus due to blockage of arachnoid granulations (requires a lumbar drain)
Hyponatraemia

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74
Q

summary of subarachnoid haemorrhages

A

Rupture of the arteries forming the circle of Willis
Often because of berry aneurysms
Sudden onset severe headache, photophobia and reduced consciousness
Thunderclap headache
Rapidly fatal, the commonest source of organs for transplant since seat belts were made compulsory

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75
Q

complications of base of skull fractures

A

may cause lower cranial nerves palsies or CSF discharge from the nose or ear

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76
Q

What are cerebral contusions

A

Bruises on the surface of the brain
Occur when the brain suddenly moves within the cranial cavity and is crushed against the skull
Typically, there is injury at the site of impact and at the site diagonally opposite this point
Oozing of blood into the brain parenchyma and associated cerebral oedema are important contributors to raised intracranial pressure

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77
Q

Subdural haemorrhage

A

Bleeding from bridging veins between cortex and venous sinuses, resulting in accumulating haematoma. Common where the patient has a small brain (alcoholics, dementia).

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78
Q

pathology of subdural haemorrhage

A

Due to haemorrhage between the dura and the arachnoid.
Results from tearing of delicate bridging veins that traverse the subdural space to drain into the cerebral venous sinuses
Blood from these veins spread freely through the subdural space, enveloping the entire cerebral hemisphere on the side of the injury

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79
Q

Causes of subdural haemorrhage

A

Minor trauma up to 9 months previously
Without trauma e.g. Dural metastases, lowered intracranial pressure

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80
Q

symptoms of subdural haemorrhage

A

Fluctuating level of consciousness
Insidious physical or intellectual slowing
Sleepiness, headache, personality change, unsteadiness

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81
Q

signs of subdural haemorrage

A

Raised Intracranial pressure (massive increase in oncotic and osmotic pressure sucks water into the haematoma, gradual rise in ICP)
Seizures
Localising neurological symptoms e.g. unequal pupils

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82
Q

Differential diagnoses for subdural haemorrhage

A

Stroke
Dementia
CNS masses e.g. tumours, abscesses

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83
Q

investigations for subdural haemorrhage

A

Imaging: CT/ MRI shows clot, with/without midline shift
Look for crescent-shaped collection of blood over 1 hemisphere.
The sickle-shape differentiates subdural blood from extradural haemorrhage.

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84
Q

management of subdural haemorrhage

A

Reverse clotting abnormalities urgently
IV mannitol to decrease ICP
Surgical management depends on the size of the clot, its chronicity, and the clinical picture;
Generally, those >10mm or with midline shift >5mm need evacuating
Address the cause of the trauma

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85
Q

extradural haemorrhage

A

Bleeding from middle meningeal artery (between bone and dura) with a characteristic lucid period.

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86
Q

pathology of extradural haemorrage

A

Due to haemorrhage between the dura and the skull
The bleeding vessel is often the middle meningeal artery which is torn following fracture of the squamous temporal bone
Accumulation of extradural blood is slow, as the firmly adherent dura is slowly peeled away from the inner surface of the skull.

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87
Q

causes of extradural haemorrhage

A

Suspect after any traumatic skull fracture.
Often due to a fractured temporal or parietal bone causing laceration of the middle meningeal artery and vein, typically after trauma to a temple just lateral to the eye.
Any tear in a dural venous sinus will also result in an extradural bleed. Blood accumulates between bone and dura.

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88
Q

clinical presentations of extradural haemorrhage

A

Patients may appear well for several hours following a head injury but then quickly deteriorate as the haematoma enlarges and compresses the brain.
The lucid interval may last a few hours to a few days before a bleed declares itself by low GCS (Glasgow coma scale) from rising ICP.
Increasingly severe headache, vomiting, confusion and seizures follow
If bleeding continues, the ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops and breathing becomes deep and irregular
Death follows a period of coma and is due to respiratory arrest (tentorial herniation)

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89
Q

differential diagnosis for extradural haemorrhage

A

Epilepsy
Carotid dissection
Carbon monoxide poisoning

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90
Q

investigations for extradural haemorrhage

A

CT shows a haematoma – biconvex (lemon shaped), hyperdense haematoma
Skull X-ray may be normal or show fracture lines crossing the course of the middle meningeal vessels

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91
Q

Management of extradural haemorrhage

A

Stabilise and transfer urgently to a neurosurgical unit for clot evacuation
IV mannitol
Care of the airway in an unconscious patient and measures to lower ICP often require intubation and ventilation

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92
Q

epilepsy

A

A recurrent tendency to spontaneous episodes of abnormal electrical activity within the brain which manifest as seizures.

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93
Q

3 Classifications of epileptic seizures

A

Partial seizures
Generalised seizures
Focal seizures

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94
Q

What are partial seizures

A

Features attributable to a localised part of one hemisphere

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95
Q

difference between simple and complex partial seizures

A

In simple partial seizures, consciousness is unimpaired (e.g. a focal motor seizure)
In complex partial seizures, consciousness is impaired (e.g. motionless staring)

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96
Q

what are generalized seizures

A

originating at some point within, and rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge with no localising features referable to a single hemisphere.

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97
Q

What are absence seizures

A

type of generalized seizure
Absence seizures cause brief (<10s) pauses, e.g. stopping talking in mid-sentence and then carrying on where left off

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98
Q

what are tonic-clonic seizures

A

type of generalized seizures
cause sudden loss of consciousness with stiffening (tonic) of limbs and then jerking (clonic)

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99
Q

What are myoclonic jerks

A

sudden violent movement of the limbs

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100
Q

What are focal seizures

A

originating within networks linked to one hemisphere and often seen with underlying structural disease.

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101
Q

3 subclasses of focal seizures

A

Without impairment of consciousness
With impairment of consciousness
bilateral, convulsive seizure

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102
Q

focal seizures without impairment of consciousness

A

awareness is unimpaired, autonomic, or psychic symptoms. No post-ictal symptoms.

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103
Q

focal seizures With impairment of consciousness

A

awareness is impaired, either at seizure onset or following a simple partial aura. Most commonly arise from temporal lobe; post-ictal confusion.

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104
Q

bilateral convulsive focal seizures

A

the electrical disturbance, which starts focally, spreads widely, causing a generalised seizure, which is typically convulsive.

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105
Q

cause of epilepsy

A

Very often idiopathic with no clear cause found
May be associated with underlying structural lesions (trauma, neoplasms, malformations), metabolic conditions (alcohol, electrolyte disorders), infections, and rare genetic diseases (e.g. ion channel mutations)

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106
Q

prodomes in epilepsy

A

Some patients may experience a preceding prodrome (an early sign or symptom) lasting hours or days in which there may be a change in mood or behaviour.

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107
Q

Aura in epilepsy

A

prodrome that implies a focal seizure, often from the temporal lobe. May be a strange feeling in the gut or flashing lights.

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108
Q

post-ictal presentation of epilepsy

A

altered state of consciousness after an epileptic seizure
Headache
Confusion
Myalgia (pain in a muscle or group of muscles).

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109
Q

clinical presentation for temporal lobe seizure

A

emotional disturbance, dysphasia, hallucinations, bizarre associations

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110
Q

clinical presentation of frontal lobe seizures

A

motor features such as peddling movements of the legs. Motor arrest, dysphasia or speech arrest.
Post-ictal Todd’s Palsy

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111
Q

what is post ictal Todd’s palsy

A

Paralysis of the limbs involved in a seizure for several hours

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112
Q

clinical presentation of parietal lobe seizure

A

sensory disturbances – tingling, numbness, pain. Motor symptoms

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113
Q

clinical presentation of occipital lobe seizure

A

visual phenomena such as spots, lines, flashes

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114
Q

differential diagnosis for seizure

A

Migraine
TIA
Cardiogenic syncope
Parasomnia

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115
Q

how to diagnose epilepsy

A

Take a thorough history: include a detailed description from a witness
Ask specifically about tongue biting and a slow recovery
Are there any triggers e.g. alcohol, stress, flickering lights
Establish the type of seizure – focal or generalised
Rule out provoking causes

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116
Q

provoking causes for seizure

A

Trauma
Stroke
Haemorrhage
Alcohol or benzodiazepine withdrawal
Metabolic disturbance

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117
Q

1st line investigation for focal epilepsy

A

Electroencephalogram (supportive not diagnostic, can determine type of epileptic syndrome)
MRI/CT (examine hippocampus, rule out other causes, e.g., tumour, bleeding)
Bloods (rule out other causes - FBC, Ca2+, electrolytes, U&Es, LFTs, glucose)
Genetic testing

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118
Q

gold standard investigations for focal epilepsy

A

Clinical diagnosis (at least 2 seizures more than 24hours apart) and EEG (focal spikes or sharp waves in affected area)

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119
Q

management for focal epilepsy

A

Usually only started after 2nd epileptic episode.
1st line – lamotrigine/carbamazepine. 2nd line – sodium valproate/levetiracetam

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120
Q

1st line investigations for generalised epilepsy

A

Electroencephalogram (supportive not diagnostic, can determine type of epileptic syndrome, e.g., 3Hz spike in absence seizure)
MRI/CT (examine hippocampus, rule out other causes, e.g., tumour, bleeding)
Bloods (rule out other causes - FBC, Ca2+, electrolytes, U&Es, LFTs, glucose)
Genetic testing (e.g., for juvenile myoclonic epilepsy)

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121
Q

gold standard investigations for generalised epilepsy

A

Clinical diagnosis (at least 2 seizures more than 24hours apart) and EEG (determine type of seizure)

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122
Q

management of generalised epilepsy

A

Usually only started after 2nd epileptic episode.
1st line – sodium valproate for all generalised seizures in males and women not childbearing age.

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123
Q

generalised epilepsy treatment for women of childbearing age

A

Women of childbearing age: give lamotrigine for all generalised seizures except myoclonic (levetiracetam/topiramate) and absence (ethosuximide). Sodium valproate highly teratogenic

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124
Q

atonic seizures

A

sudden loss of muscle tone causing a fall, no LOC

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125
Q

non drug epilepsy therapies

A

Psychological therapies
Relaxation
CBT
Do not improve seizure frequency
Surgical intervention
Neurosurgical resection
Vagus nerve stimulation is a palliative treatment option for refractory epilepsy

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126
Q

what is Dementia

A

A neurodegenerative syndrome with progressive decline in several cognitive domains.

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127
Q

4 types of dementia

A

Alzheimer’s, Lewy body, Parkinson’s, vascular

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128
Q

features of vascular dementia

A

Cumulative effect of many small strokes.
Sudden onset and stepwise deterioration is characteristic.

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129
Q

features of lewy body dementia

A

Fluctuating cognitive impairment, detailed visual hallucinations, parkinsonism
Histology is characterised by Lewy bodies in brainstem and neocortex

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130
Q

features of fronto-temporal dementia

A

Frontal and temporal atrophy with loss of >70% of spindle neurons.
Patients may display executive impairment – behavioural/ personality change, disinhibition, hyperorality, emotional unconcern.

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131
Q

10 causes of dementia

A

Lewy body, Parkinson’s, vascular,Familial autosomal dominant Alzheimer’s

Alcohol/ drug abuse
Repeated head trauma
Pellagra – lack of nicotinic acid
Whipple’s disease – GI malabsorption
Huntington’s

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132
Q

history taking for dementia

A

ask about timeline of decline and the domains affected. Non-cognitive symptoms such as agitation, aggression, or apathy indicate late disease

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133
Q

cognitive testing for dementia

A

use a validated dementia screen such as the AMTs or similar, plus short tests of executive function and language.
Carry out a mental state examination to identify anxiety, depression or hallucinations

134
Q

examination for dementia

A

identify a physical cause, risk factors (e.g. for vascular dementia) or parkinsonism.

135
Q

why conduct a medication review for dementia diagnosis

A

important to exclude drug-induced cognitive impairment

136
Q

what is the 6CIT Dementia test

A

Six item cognitive impairment test
What year is it?
What month is it?
Give an address with 5 parts (John, Smith, 42, High, St, Bedford)
Count 20-1
Say months of year in reverse
Repeat address

137
Q

investigations for dementia

A

Look for reversible/ organic causes: raised TSH/low B12/folate
Check MSU, FBC, ESR, U&E, LFT and glucose.
MRI can identify other reversible pathologies e.g. subdural haematoma, as well as underlying vascular damage or structural pathology
Functional imaging may help delineate subtypes where diagnosis is not clear

138
Q

Medication management of dementia

A

avoid drugs that impair cognition (e.g. sedatives, tricyclics)

139
Q

Non- pharmacological interventions for dementia

A

non-cognitive symptoms may respond to measures such as aromatherapy, multisensory stimulation, massage, music, and animal-assisted therapy

140
Q

what is vascular dementia

A

A disease characterised clinically by dementia and histopathologically by injury to the brain parenchyma, associated with a wide range of cerebrovascular lesions.

141
Q

presentation of vascular dementia

A

Impairment of executive function and slowing of mental processing may be prominent, particularly with diffuse subcortical involvement.
May be difficult to capture on standard cognitive testing (Mini-mental state examination, MMSE)
May present with stepwise progression (multi-infarct dementia) and focal neurology (depending on infarct location)

142
Q

presentation of dementia with lewy bodies

A

Progressively worsening dementia very similar to Alzheimer’s disease
Useful distinguishing features from Alzheimer’s disease include fluctuating levels of cognition, recurrent visual hallucinations, features of parkinsonism, and hypersensitivity to neuroleptics
Autonomic nervous system problems and sleep disorders are also described

143
Q

Alzheimer’s disease

A

A neurodegenerative disease characterised clinically by dementia and histopathologically by neuronal loss in the cerebral cortex, in associated with numerous amyloid plaques and neuro-fibrally tangles.

144
Q

Aetiology of alzheimers

A

Environmental and genetic factors play a role
Accumulation of β-amyloid peptide, a degradation product of amyloid precursor protein, results in progressive neuronal damage, neurofibrillary tangles, raised number of amyloid plaques and loss of acetylcholine.
Neuronal loss is selective – the hippocampus, amygdala, temporal neocortex, and subcortical nuclei are most vulnerable.

145
Q

pathology of alzheimers

A

extracellular deposition of beta-amyloid plaques, tau-containing intracellular neurofibrillary tangles, damaged synapses, atrophy, cortical scarring, decreased Ach neurotransmitter.

146
Q

temporal lobe functions

A

Hearing (superior temporal lobe)
Language comprehension (superior temporal lobe)
Semantic knowledge (anterior temporal lobe)
Memory (hippocampus)
Emotional/ effective behaviour (limbic system)

147
Q

early presentation of alzheimers

A

Begins with memory loss, particularly day-to-day memory and new learning, which correlates with the early involvement of the medial temporal lobe and the hippocampus.
Episodic memory: frequent intrusions and repetition errors, and high numbers of false positive errors in recall

148
Q

later stage presentation of alzheimers

A

Over time, there is increasing disability in managing daily activities such as finances and shopping
Agnosia – not being able to recognise self in the mirror
Psychotic symptoms: delusions (delusions of theft) or hallucinations
Loss of motor skills then causes difficulty dressing, cooking and cleaning
Late in the disease, there is agitation, restlessness, wandering and disinhibition.
This may cause considerable upset to the family and carers.

149
Q

terminal stage presentations of dementia

A

reduced speech, immobility, and incontinence.

150
Q

differential diagnosis of alzheimers

A

Vascular/mixed dementia
Dementia with Lewy bodies
Depressive pseudo dementia

151
Q

1st line investigation for alzheimers

A

MMSE (mini mental state examination): score /30. >25 = normal. 18-25 = impaired. <18 = severely impaired. Tests communication, memory, activities of daily life.
memory clinic assessment, Bloods – FBC, U&Es, B12 (rule out other causes), brain MRI

152
Q

gold standard investigation for alzheimers

A

Brain MRI (temporal lobe and cortical atrophy)

153
Q

prevention of alzheimers

A

Socially active
Cognitively active
Control vascular risk factors
Treat mood and anxiety

154
Q

medication for alzheimers

A

Acetyl choline esterase inhibitors e.g. Rivastigmine
Memantine (anti-glutamate)
Antipsychotics – consider only if severe e.g. extreme agitation/ psychosis

155
Q

Parkinsons

A

A neurodegenerative hypokinetic movement disorder characterised clinically by parkinsonism and histologically by neuronal loss and Lewy bodies concentrated in the substantia nigra.

156
Q

pathology of parkinsons

A

Neurones from the substantia nigra connect to the putamen and globus pallidus where they release dopamine and control movement
Lack of dopamine release results in movement disorder (loss of dopaminergic neurons in substantia nigra)
It is recognised that other parts of the nervous system are involved, resulting in additional symptoms
Most cases are sporadic, though multiple genetic loci have been identified in familial cases

157
Q

classical triad of parkinsons manifestations

A

Tremor. Worse at rest; often ‘pill-rolling’ of thumb over fingers
Rigidity. Hypertonia: rigidity and tremor give cogwheel rigidity felt during rapid pronation/supination
Bradykinesia (parkinsonism): slow to initiate movement. Shuffling, pitched forward gait

158
Q

clinical manifestations of parkinsons

A

Onset is typically unilateral
Tremor.
Rigidity
Bradykinesia ]Autonomic dysfunction, cognitive neurobehavioral disturbances, and sleep dysfunction are also common
Rapid eye movement (REM) sleep behaviour disorder may precede parkinsonism
Dysphagia may be seen with disease progression
Patients may develop dementia and depression - debilitating

159
Q

differential diagnosis for parkinsons

A

Cerebellar disease
Fronto-temporal dementia

160
Q

1st line investigations for parkinsons

A

dopaminergic agent trial

161
Q

3 step diagnosis of parkinsons

A
  1. Diagnosis of parkinsonian syndrome: bradykinesia + one of rigidity, resting tremor, or postural instability
  2. Exclusion criteria (none to be met): Hx stroke, repeated head injury, neuroleptic treatment, unilateral features after 3 years, cerebellar signs, Babinski’s sign, early severe dementia, negative response to large L-dopa dose.
  3. Supportive criteria (3+ required): unilateral onset, rest tremor present, progressive, excellent response to L-dopa, visual hallucinations.
162
Q

pharmacological management of parkinsons

A

Treatment with dopaminergic drugs eases symptoms of parkinsonism but does not slow the progression of the disease.
Co-careldopa – levodopa and carbidopa
Pramiprexole/ ropinirole – dopamine receptor agonists
Tremor management – anticholinergic such as amantadine.

163
Q

problem with levodopa use

A

Patients on long term treatment with levodopa develop severe dyskinesias (involuntary jerking movements) as a side effect

164
Q

management of selected parkinsons patients with severe tremor

A

Deep brain stimulation of the subthalamic nucleus works by rebalancing aspects of the basal ganglia circuit and is helpful in a small number

165
Q

huntingtons chorea

A

An inherited neurodegenerative disorder caused by mutation of the HTT gene

166
Q

genetics of huntingtons

A

HTT contains a sequence of CAG trinucleotide repeats (chromosome 4) which usually number <36
Mutant HTT has >36 trinucleotide repeats. The higher the number of trinucleotide repeats, the fuller the penetrance and the younger the age of onset
Instability of the repeat sequences tends to result in their expansion in each successive generation, a phenomenon known as anticipation

167
Q

pathology of huntingtons

A

Huntingtin, the protein coded by HTT, interacts with many other proteins and has many biological functions. It is expressed in all cells but is present in highest concentration in the brain and testis
Mutated huntingtin is thought to be cytotoxic to certain cell types, most notably neurones in the caudate nucleus and putamen
Atrophy and neuronal loss of striatum and cortex
Loss of neurotransmitters, including GABA, acetylcholine and glutamate.

168
Q

clinical manifestation of huntingtons

A

Decrease of GABA and unbalanced dopamine activity result in chorea - Uncontrolled, random, jerky movements
Over time, there is motor, neuropsychiatric, and cognitive decline, ultimately terminating in dementia

169
Q

differential diagnoses for huntingtons

A

SLE
Multiple sclerosis

170
Q

investigations of huntingtons

A

Clinical diagnosis.
MRI/CT brain – loss of striatal volume. Genetic testing (>35 CAG repeats on chromosome 4)

171
Q

clinical diagnosis of huntingtons

A

Abnormal eye movements
Problems with initiating saccades
Broken pursuit
Chorea
Random, unpredictable movements
Often additional touch of parkinsonism
Rigidity
Slowness of fine finger movements

172
Q

management of huntingtons

A

Chorea – antipsychotics: risperidone (dopamine receptor antagonists)
Depression – selective serotonin reuptake inhibitors: sertraline
Psychosis – neuroleptics: haloperidol
Aggression – antipsychotics: risperidone

173
Q

3 types of primary headaches

A

Migraine, cluster, tension type

174
Q

6 types of secondary headaches

A

Meningitis, subarachnoid haemorrhage, GCA, idiopathic intracranial hypertension, medication overuse headache

175
Q

Headache history markers needing further investigation

A

> 50
Hx of HIV or cancer or trauma or risk factors cerebral vein sinus thrombosis
Changing personality or cognitive dysfunction
Vomiting without other obvious cause

176
Q

headache features which indicate need for further investigation

A

Jaw claudication (pain associated with chewing) or visual disturbance
Severe eye pain – closed angle glaucoma
Changing in frequency, characteristics or associated symptoms
Postural
Sudden onset headache/ thunderclap
Exercise or Valsalva (e.g. coughing, laughing, straining)
Focal neurological symptoms (e.g. limb weakness, unusual area aura <5 min or >1hr)

177
Q

features of a headache exam indicating need for further investigation

A

Fever
Altered consciousness
Neck stiffness
Other abnormal neurological examination

178
Q

5 headache features indicating immediate referral

A

Thunderclap headache
Seizure and new headache
Suspected encephalitis
Red eye – acute glaucoma
Headache + new focal neurology – including papilledema

179
Q

4 cancer red flags for headache

A

new onset + history of cancer, papilledema, cluster headache

180
Q

questions needed in a headache history

A

Types/number – history for each one
Time – onset/duration/how long/why now/ frequency and pattern
Pain – severity/quality/site and spread
Associated – N/V/P/P/cranial autonomic features
Triggers +/- - triggers/ aggravating/ relieving/ FHx
Response – during attack/ function/ medication useful
Between attacks – normal/persisting symptoms
Any change in attacks

181
Q

Migraine

A

A recurrent throbbing headache that typically affects one side of the head and is often accompanied by nausea and disturbed vision.

182
Q

risk factors for migraine

A

Smoking
Age >35 yrs
High blood pressure
Obesity/ diabetes mellitus
Oral contraceptive pill

183
Q

potential triggers for migraines

A

CHOCOLATE
Chocolate
Hangovers
Orgasms
Cheese/ caffeine
Oral contraceptives
Lie-ins
Alcohol
Travel
Exercise

184
Q

clinical presentation of migraine

A

Visual or other aura lasting 15-30min followed within 1h by unilateral, throbbing headache
Isolated aura with no headache
Episodic severe headache without aura, often premenstrual, usually unilateral, with nausea, vomiting
Allodynia – all stimuli produce pain (brushing hair/wear earrings/glasses)

185
Q

differential diagnoses for migraine

A

Cluster or tension headache
Cervical spondylosis
Intracranial pathology
TIAs

186
Q

investigations for migraine

A

1st line+ GS= clinical diagnosis

187
Q

diagnosis criteria for migraine

A

if no aura:
>5 headaches lasting 4-72hours + nausea/vomiting + any 2 of;
Unilateral
Pulsating
Impairs routine activity

188
Q

management of migraines

A

Avoid identified triggers and ensure analgesic rebound headache is not complicating matters
Prophylactic treatment: reduced attack frequency – propranolol
Treatment during an attack: oral triptan (Severe) combined with either an NSAID (mild) or paracetamol
Non-pharmacological therapies: warm or cold packs to the head or rebreathing into paper bag may help abort attacks.
Transcutaneous nerve stimulation may help

189
Q

What are tension headaches

A

Primary headache. Most common chronic and recurrent daily headache. Bilateral generalised pain, can spread to neck. Can be episodic <15 days/per month, or chronic >15 days/month (for at least 3 months)

190
Q

9 triggers for tension headaches

A

stress, sleep deprivation, bad posture, hunger, eyestrain, anxiety, noise, overexertion, tension in muscles of face/jaw/neck

191
Q

clinical presentations for tension headaches

A

At least one of: bilateral, pressing/tight and non-pulsatile (like an elastic band around head), mild/moderate intensity, +/- scalp tenderness.
No aura, vomiting or head sensitivity to movement.
Can be some ‘pressure’ behind eyes, but pain isn’t localised around eye

192
Q

investigations for tension headaches

A

1st line+ GS= clinical diagnosis
If suspected pathology: CT sinus, MRI brain, lumbar puncture

193
Q

differential diagnoses for tension headaches

A

Migraine, cluster headache, giant cell arteritis, sphenoid sinusitis

194
Q

management of tension headaches

A

Avoid triggers and stress relief. Symptomatic relief: aspirin, paracetamol, ibuprofen, AVOID OPIOIDS
Chronic: antidepressants (amitriptyline)
Limit analgesics to no more than 6 days per month to reduce the risk of medication-overuse headaches

195
Q

cluster headache clinical manifestations

A

Rapid-onset of excruciating pain around one eye that may become watery and bloodshot with lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis.
Pain is strictly unilateral and almost always affects the same side.
It lasts 15-180min, occurs once or twice a day, and is often nocturnal.
Clusters last 4-12 weeks and are followed by pain-free periods of months or even 1-2 years before the next cluster

196
Q

treatment of cluster headaches

A

Acute attack: give 100% O2 for 15 min via non-rebreathable mask. Sumatriptan sc 6mg at onset

197
Q

preventative measures for cluster headaches

A

Avoid triggers: e.g. alcohol
Medication: consider corticosteroids short term e.g. prednisolone
Verapamil (CCB)

198
Q

two classes of drug overuse for headaches

A

A: Headache present on >15 days/month
B: Regular use for >3 months of one or more symptomatic treatment drugs

199
Q
A
200
Q

management of drug overuse for headaches

A

Withdraw analgesics – aspirin or naproxen may mollify the rebound headache.

201
Q

Giant cell arteritis

A

A vasculitis of medium and large vessels which preferentially affects head and neck arteries. Most patients are adults aged >50y.

202
Q

clinical manifestations of giant cell arteritis

A

Presents over weeks or months with;
Fever
Anorexia
Weight loss
Involvement of the temporal artery causes headache, scalp tenderness, and jaw claudication
Involvement of ocular vessels can cause blindness
Aortic involvement may lead to thoracic or abdominal aortic aneurysm formation

203
Q

1st line investigation for giant cell arteritis

A

Raised CRP, Raised ESR >50mm/hr. FBC (anaemia), LFT/RFT may be abnormal
Halo sign (wall thickening) on vascular ultrasonography of temporal and axillary artery

204
Q

gold standard investigation for giant cell arteritis

A

Temporal artery biopsy (shows giant cells, granulomatous inflammation – patchy lesions therefore take big sample)

205
Q

management of giant cell arteritis

A

Management;
Start prednisolone PO immediately or IV methylprednisolone if evolving visual loss
Main cause of death in giant cell arteritis is long-term steroid treatment

206
Q

trigeminal neuralgia (face pain)

A

Neuralgia involving one or more of the branches of the trigeminal nerves, and often causing severe pain.

207
Q

triggers for trigeminal neuralgia

A

Washing affected area
Shaving
Eating
Talking
Dental prostheses

208
Q

secondary causes of trigeminal neuralgia

A

Compression of the trigeminal root by anomalous or aneurysmal intracranial vessels or a tumour
Hypertension
Chronic meningeal inflammation
MS
Skull base malformation e.g. Chiari

209
Q

clinical manifestations of trigeminal neuralgia

A

Paroxysms of intense, stabbing pain, lasting seconds, in the trigeminal nerve distribution.
Unilateral, typically affecting mandibular or maxillary divisions.
The face screws up with pain

210
Q

differential diagnosis for trigeminal neuralgia

A

Migraine
Glossopharyngeal neuralgia
Sinusitis
Giant cell arteritis

211
Q

gold standard investigations for trigeminal neuralgia

A

Clinical, 3 or more attacks with same presentation (paroxysmal sharp stabbing facial pain up to 2 mins)

212
Q

management of trigeminal neuralgia

A

Carbamazepine
If drugs fail, surgery may be necessary – directed at the peripheral nerve, the trigeminal ganglion or the nerve root
Microvascular decompression: anomalous vessels are separated from the trigeminal root.

213
Q

causes for spinal cord compression

A

Secondary malignancy (breast, lung, prostate, thyroid, kidney)
Rare:
Infection
Cervical disc prolapse
Haematoma/ myeloma

214
Q

symptoms of cord compression

A

Bilateral leg weakness
Preceding back pain
Bladder (and anal) sphincter involvement is late and manifests as hesitancy, frequency and painless retention

215
Q

signs for cord compression

A

Look for a motor, reflex, and sensory level, with normal findings above the level of the lesion
LMN signs at the level
UMN signs below the level

216
Q

differential diagnosis for cord compression

A

Transverse myelitis
MS
Carcinomatous meningitis
Cord vasculitis

217
Q

1st line investigations for cord compression

A

X-ray whole spine, MRI spine, RFTs, haemoglobin – monitor blood loss

218
Q

gold standard investigation for cord compression

A

MRI spine (visualise cord compression)

219
Q

management for cord compression

A

Give urgent dexamethasone in malignancy while considering more specific therapy e.g. radiotherapy or chemotherapy
If reduced mobility consider thromboprophylaxis – compression stockings, LMWH
Epidural abscesses must be surgically decompressed, and antibiotics given

220
Q

cauda equina syndrome

A

Spinal cord compression at the site of the cauda equina.

221
Q

causes of cauda equina syndrome

A

Secondary malignancy (breast, lung, prostate, thyroid, kidney)
Rare:
Infection
Haematoma/ myeloma
congenital lumbar disc disease and lumbosacral nerve lesions

222
Q

signs of cauda equina syndrome

A

Back pain and radicular pain down the legs;
Asymmetrical, atrophic, areflexic paralysis of the legs
Sensory loss in a root distribution
Decreased anal sphincter tone on PR, bladder/bowel incontinence

223
Q

multiple sclerosis

A

A relapsing and remitting demyelinating disease of the CNS, in which episodes of neurological disturbance affect different parts of the CNS at different times.

224
Q

pathology of MS

A

Episodes of demyelination lead to attacks of acute neurological deficit, which develop over a period of a few days and remain for a few weeks before symptom recovery
In the early stages of the disease, complete or almost complete recovery from an episode of demyelination is typical
As the diseases progresses, recovery is slower and residual deficit remains as a critical threshold of axonal death.
Eventually, extensive axonal death results in permanent neurological disability, characteristic of progressive disease

225
Q

clinical presentations of MS

A

Symptoms may be highly variable, depending on the lesion site in the CNS
Blurred vision/ loss of colour vision due to optic nerve demyelination
Vertigo and incoordination due to cerebellar demyelination
Eye movement disorders due to brainstem demyelination
Unilateral optic neuritis (pain on eye movement and reduced rapid central vision)
Patchy numbness and tingling in a limb, with progression to paraplegia, incontinence, and sexual dysfunction due to spinal cord demyelination
Symptoms worsen with heat – Uhthoff’s phenomenon

226
Q

relapsing/remitting patient features for MS

A

Random attacks over a number of years
More frequent in the first 3 – 4 years
Recovery varies markedly among patients and from one attack to the next
Disabilities often accumulate with each successive attack

227
Q

primary/secondary chronic progressive MS features

A

Slow, inexorable decline in neurological functions
From disease onset
Following an initial relapsing/ remitting course

228
Q

benign chronic progressive MS features

A

Few relapses
Little disability

229
Q

differential diagnoses for MS

A

Infectious disease - Lyme disease
Autoimmune disorders – SLE, primary Sjogren’s syndrome

230
Q

first line investigations for MS

A

Bloods should be normal: FBC, U&Es, LFTs, TFTs, B12, HIV serology, calcium, glucose.
Lumbar puncture (oligoclonal IgG bands in CSF), MRI, evoked potentials (measures brain electrical activity in response to stimulation of sight, sound or touch).

231
Q

Gold standard investigations for MS

A

McDonald criteria: symptoms disseminated in time (>1 month apart) and space (damage to different parts of CNS seen on MRI). GS tool = MRI brain and spinal cord

232
Q

General management of MS

A

MDT care, supportive therapy, legal obligation to inform DVLA.

233
Q

Management of acute relapses of MS

A

steroids (IV methylprednisolone).

234
Q

management of relapsing remitting MS

A

interferon beta (CI in pregnancy), DMARDs, biologics (IV natalizumab), oral fingolimod (immunomodulator)

235
Q

Management of secondary progressive MS

A

Siponimod or methylprednisolone.

236
Q

management of primary progressive MS

A

ocrelizumab (DMARD)

237
Q

symptom control for MS

A

Spasticity – baclofen
Tremor – botulinum toxin type A injections improve arm tremor and functioning
Urgency/ frequency – teach intermittent self-catheterisation
Fatigue – amantadine, CBT, exercise.

238
Q

Myasthenia gravis- NMJ disorder

A

An autoimmune disease caused by production of autoantibodies directed against various antigens of the neuromuscular junction - typically the nicotinic acetylcholine receptor

239
Q

aetiology of myasthenia gravis

A

Precisely what leads to the production of the autoantibodies is unclear
Up to 75% of patients with nAChR autoantibodies have an abnormality of the thymus, either a neoplasm (thymoma) or hyperplasia.

240
Q

Pathology of myasthenia gravis

A

The nAChR is the receptor at the motor endplate, through which the neurotransmitter acetylcholine acts to stimulate muscular contraction.
Autoantibodies binding to the nAChR limit depolarisation at the endplate and thus impair muscular contraction
MuSK is involved with clustering of nAChR, which is important for its normal function

241
Q

clinical manifestations of myasthenia gravis

A

The key feature is muscular fatigability
Symptoms can be very subtle, and the diagnosis is easily missed or mistaken for other conditions.

242
Q

muscle groups affected by myasthenia gravis

A

in order, are extraocular, bulbar face, neck, limb girdle, and trunk

243
Q

What is lambert- eaton syndrome

A

typically a paraneoplastic syndrome and patients develop autoantibodies against voltage-gated calcium channel on the presynaptic nerve terminal.

244
Q

symptoms of lambert-eaton syndrome

A

Gait difficulty before eye signs
Autonomic involvement (dry mouth, constipation, impotence
Hyporeflexia and weakness, which improve after exercise

245
Q

differential diagnosis for myasthenia gravis

A

Polymyositis/ other myopathies
SLE
Takayasu’s arteritis

246
Q

investigations for myasthenia gravis

A

Antibodies: increased anti-AChR antibodies, -ve look for MuSK antibodies
EMG: decremental muscle response to repetitive nerve stimulation
Imaging: CT to exclude thymoma

247
Q

management of Myasthenia gravis

A

Combination of acetylcholinesterase inhibitors (such as pyridostigmine) and immunomodulatory therapies.
Immunosuppression: treat relapses with prednisolone

248
Q

myasthenic crisis

A

Life-threatening weakness of respiratory muscles during a relapse.
Can be difficult to differentiate from cholinergic crisis.
Monitor forced vital capacity
Ventilatory support may be needed. Treat with plasmapheresis or IVIg and identify and treat the trigger for the relapse (e.g. infection, medications)

249
Q

motor neuron disease

A

A group of neurodegenerative diseases characterised by selective loss of motor neurones.

250
Q

4 clinical patterns for MND

A

ALS/ amyotrophic lateral sclerosis. Loss of motor neurons in motor cortex and the anterior horn of the cord, so combined UMN + LMN signs.
Progressive bulbar palsy. Only affects cranial nerves IX-XII
Progressive muscular atrophy. Anterior horn cell lesion, so LMN signs only. Affects distal muscle groups before proximal.
Primary lateral sclerosis. Rare. Loss of Betz cells in motor cortex: mainly UMN signs, marked spastic leg weakness and pseudobulbar palsy. No cognitive decline.

251
Q
A
252
Q

Clinical manifestations of MND

A

Asymmetric weakness, wasting, fasciculation, and spasticity of limb muscles
Difficulty swallowing, chewing, speaking, coughing, and breathing
Cognitive changes may also occur (overlap with frontotemporal dementia)

253
Q

Clinical features of lower motor neurone lesions

A

Muscle tone normal or reduced (flaccid)
Muscle wasting
Fasciculation – visible spontaneous contraction of motor units
Reflexes depressed or absent
Everything goes down!!!

254
Q

clinical features of upper motor neurone pathology

A

Muscle tone is increased (spasticity)
Tendon reflexes/ jaw jerk are brisk
Extensor Plantar response (+Babinski sign)
Characteristic pattern of limb muscle weakness (pyramidal pattern)
Emotional lability may be present
Everything goes up!!!

255
Q

What is the Characteristic pattern of limb muscle weakness (pyramidal pattern) for upper motor neurone pathology

A

Upper limbs extensor muscles weaker than flexors
Lower limbs flexors weaker than extensors
Finer more skilful movements most severely impaired

256
Q

differential diagnosis for MND

A

Multifocal motor neuropathy with conduction block
Bulbospinal muscular atrophy (Kennedy syndrome)
Motor neuropathies

257
Q

investigations for MND

A

There is no diagnostic test.
Brain/ cord MRI helps exclude structural causes, LP helps exclude inflammatory ones
Neurophysiology can detect subclinical denervation and help exclude mimicking motor neuropathies.

258
Q

Management of MND

A

The disease is usually progressive and fatal within a few years
Adopt a multidisciplinary approach: neurologist, palliative nurse, hospice, physio, speech therapist, dietician, social services
Riluzole (an inhibitor of glutamate release and NMDA receptor antagonist) is the only medication shown to improve survival.
Dysphagia: blend food. Gastrostomy is an option
Spasticity: exercise, orthotics
Communication difficulty: provide augmentative and alternative communication equipment
End of life care: involve palliative care team from diagnosis

259
Q

Guillain-Barre syndrome

A

Classical Guillain-Barre syndrome (GBS) is an acute demyelinating polyneuropathy which usually follows 1-2 weeks after an upper respiratory tract or GI infection.

260
Q

Aetiology of GBS

A

Common triggers are Clostridium jejuni, Mycoplasma, CMV, HIV, VZV, and EBV
Other associations include vaccination, surgery, and malignancy
In many cases, no clear cause can be identified

261
Q

pathology of GBS

A

Theories suggest that the immune response mounted to an antigen on a pathogen cross-reacts with components of the peripheral nerve, particularly myelin
Demyelination leads to an acute polyneuropathy

262
Q

clinical manifestitions of GBS

A

A few weeks after an infection a symmetrical ascending muscle weakness starts
Sudden onset of tingling and numbness of fingers and toes
Over a period of weeks, the weakness spreads proximally
Classical form is acute inflammatory demyelinating polyneuropathy (AIDP). Antibodies to gangliosides, basal lamina components, and several myelin proteins

263
Q

investigations for GBS

A

Lumbar puncture typically shows increased CSF protein with a normal cell count – progressive ventilatory failure is the main danger and ventilatory support may be required

264
Q

management of GBS

A

IV immunoglobulin

265
Q

division of chronic neuropathies

A

small fibre and larger fibre

266
Q

division of larger fibre neuropathies

A

axonal or demyelinating

267
Q

4 common mononeuropathies

A

Carpal tunnel syndrome (median nerve)
Ulnar neuropathy (entrapment at the cubital tunnel)
Peroneal neuropathy (entrapment at the fibular head)
Cranial mononeuropathies (III or VII cranial nerve palsy)

268
Q

3 causes of mononeuropathies

A

Idiopathic
Immune mediated
Ischaemic

269
Q

Ataxia

A

Poor balance
Sensory (loss of proprioception) or cerebellar
When sensory, ataxia gets worse with eyes closed or when dark

270
Q

motor symptoms of peripheral neuropathies

A

Muscle cramps
Weakness
Fasciculations – muscle twitches
Atrophy
High arced feet (pes cavus)

271
Q
A
272
Q
A
273
Q
A
274
Q
A
275
Q

1st line investigations for PN

A

Bloods – FBC, glucose, U&Es, LFTs, TFTs, B12, ESR.
Nerve conduction studies. Electromyography (measures muscle electrical activity). Nerve biopsy.

276
Q

GS investigation for PN

A

Nerve conduction studies

277
Q

olfactory nerve lesion presentation

A

impaired/lost sense of smell

278
Q

optic nerve lesion presentation

A

blindness, visual field defects

279
Q

oculomotor lesion presentation

A

ptosis, down + out eye, fixed dilated pupil

280
Q

trochlear lesion presentation

A

diplopia looking down, always due to trauma

281
Q

trigeminal lesion presentation

A

jaw deviates to affected side, loss of corneal reflex, causes: trigeminal neuralgia: sensory pain/motor jaw pain in V1/2/3

282
Q

abducens lesion presentation

A

adducted eye, inability to look laterally, sign of raised ICP

283
Q

facial lesion presentation

A

facial droop with forehead sparing, causes: bell’s palsy, parotid inflammation

284
Q

vestibulocochlear lesion presentation

A

hearing loss, loss of balance, causes: skull changes, (e.g., Paget’s), compression, middle ear disease

285
Q

glossopharyngeal lesion presentation

A

impaired gag reflex

286
Q

vagus lesion presentation

A

impaired gag reflex, swallowing, respiration, vocal issues, causes: jugular foramen lesion

287
Q

accessory lesion presentation

A

can’t shrug shoulders or turn head against resistance

288
Q

hypoglossal lesion presentation

A

tongue deviation towards affected side

289
Q

investigations for cranial nerve lesions

A

Neurological examination, MRI

290
Q

types of primary brain tumour

A

gliomas – astrocytoma (most common), oligodendroglioma. Others – ependymoma, meningioma, schwannoma, craniopharyngiomas

291
Q

types of secondary brain tumours

A

non-small cell lung cancers (most common), small cell lung cancer, breast, melanoma, renal cell carcinoma, GI

292
Q

pathophysiology of gliomas

A

tumours of glial cells of brain and spinal cord

293
Q

key presentations of brain tumours

A

Raised ICP, Cushing triad (bradycardia, raised pulse pressure, irregular breathing), focal neurology, epileptic seizures, lethargy, weight loss, papilloedema (swelling of optic disc), CN6 palsy.

294
Q

gold standard investigations for brain tumours

A

MRI head to locate tumour then biopsy to determine grade
No LP due to raised ICP- big Contraindication

295
Q

management of brain tumours

A

1st line – surgery to remove tumour and decrease ICP. + chemo before/after/during surgery
Dexamethasone + mannitol to decrease ICP

296
Q

meningitis

A

Infection of the subarachnoid space. Inflammation of the meninges.

297
Q

microbiology of meningitis

A

Viruses - usually echoviruses, EBV, herpes simplex, mumps
Most cases of bacterial meningitis are caused by Neisseria meningitidis or streptococcus pneumoniae. Escherichia coli and group B streptococci are important causes in neonates.

298
Q

4 infective causes of meningitis

A

Bacterial
Viral
Fungal
Parasitic

299
Q

3 non-infective causes of meningitis

A

Paraneoplastic
Drug side effects
Autoimmune (e.g. vasculitis/ SLE)

300
Q

3 routes of infection to the meniges

A

Extracranial infection
Neurosurgical complications
Via blood stream

301
Q

pathology of meningitis

A

Bacteria usually reach the meninges via the bloodstream from the nasal cavity, often following a viral upper respiratory tract infection
Both Meningococcus and Pneumococcus have capsules which render them resistant to phagocytosis and complement.
The bacteria enter the subarachnoid space where the blood-brain barrier is weak, e.g. the choroid plexus
Once in the CSF, the bacteria multiply rapidly and stimulate an acute inflammatory response within the meninges

302
Q

pathophysiology of menigitis

A

Blood – CSF – brain barrier
Bacteria enter CSF, and can be isolated from the immune cells due to BBB
Replication – number of bacteria increases
Blood vessels become leaky
WBCs can enter the CSF, meninges and brain
Meningeal inflammation. Brain swelling

303
Q

6 clinical menifestations of meningitis

A

Headache
Fever
Neck stiffness
Photophobia
The symptoms are usually more severe in bacterial meningitis
Non-blanching purpuric rash

304
Q

differential diagnosis for meningitis

A

“worst headache ever”
Subarachnoid haemorrhage, trauma, thunderclap onset
Flu and other viral illnesses
Sinusitis

305
Q

1st line investigations of meningitis

A

If suspected do not delay treatment – IV antibiotics before lumbar puncture. Lumbar puncture within 1 hour of arrival.
Blood cultures (positive).
FBC (leucocytosis, anaemia, thrombocytopenia),
U&E (acidosis, hypokalaemia, hypocalcaemia, hypomagnesemia),
Glucose, lactate dehydrogenase, LFTs. ABG (acidosis), clotting screen (DIC).
Pneumococcal and meningococcal PCR. Viral PCR. Fungal cultures (3 sets)

306
Q

gold standard tests for meningitis

A

Lumbar puncture (L3/L4) and CSF analysis. Contraindicated with raised ICP, shock

307
Q

results of normal LP

A

Opening pressure 90-180
Appearance Clear
WCC <8
Protein 15-45
Glucose (vs serum level) 50-80

308
Q

results of bacterial meningitis LP

A

Opening pressure Elevated
Appearance Turbid
WCC >1000-2000 neutrophils
Protein >200
Glucose (vs serum level) <40

309
Q

LP results for viral meningitis

A

Opening pressure Normal
Appearance Clear
WCC <300 lymphocytes
Protein <200
Glucose (vs serum level) Normal

310
Q

LP results for fungal meningitis

A

Opening pressure Normal-elevated
Appearance Clear
WCC <500
Protein >200
Glucose (vs serum level) Normal-low

311
Q
A
312
Q

management for meningitis

A

Viral meningitis usually runs a mild course with complete recovery
Bacterial meningitis is a much more serious, potentially life-threatening infection if not treated early with appropriate antibiotics.

313
Q

immediate management steps for meningitis

A

1.Assess GCS (Glasgow coma score)
2. Blood cultures – takes hours – days for organism to grow and be distinguished
3. Broad spectrum antibiotics
a. First line antibiotics - either ceftriaxone or cefotaxime
4. Special considerations
a. Penicillin allergies
b. Immunocompromised – risk of listeria
c. Recent travel – risk of penicillin resistance
5. Steroids
a. IV dexamethasone
b. Steroids reduce neurological sequelae and therefore reduce morbidity
6. Lumbar puncture
a. Definitive investigation to diagnose meningitis
b. Microscopy, gram stain, culture, protein, glucose, viral PCR

314
Q

encephalitis

A

Infection of the brain parenchyma. Inflammation of the brain – confusion due to direct inflammation/infection of brain.

315
Q

viral causes of encephalitis

A

Viruses are the most common cause, usually HSV
Herpes simplex
Varicella zoster
Other viral culprits: measles, mumps, rubella, EBV, HIV, CMV

316
Q

non-viral causes of encephalitis

A

Any bacterial meningitis
TB
Malaria
Lyme disease

317
Q

other causes of encephalitis

A

Japanese encephalitis virus
Tick-borne encephalitis
Rabies
West Nile virus
Non-infective – autoimmune, paraneoplastic

318
Q

pathology of HSV encephalitis

A

HSV encephalitis occurs following reactivation of the virus in the trigeminal ganglion, from which the virus can pass into the temporal lobe.

319
Q

clinical manifestations of encephalitis

A

Precedes with ‘flu-like’ illness
Confusion
Behavioural changes
Altered consciousness: low GCS or coma
Seizures in severe cases

320
Q

differential diagnosis for encephalitis

A

Meningitis
TB
Brain abscess

321
Q

1st line investigations for encephalitis

A

Bloods – FBC (raised WCC), U&Es (hyponatraemia), LFTs, TFTs, B12, lactate
Lumbar puncture and CSF analysis – viral PCR to detect virus (lymphocytosis with normal CSF:plasma glucose ratio)
Blood cultures. EEG (background slowing). HIV testing

322
Q

Gold standard investigations for encephalitis

A

MRI brain (swelling of brain)

323
Q

management of encephalitis

A

Urgent antiviral treatment
IV if HSV or VZV
Mostly supportive
Symptomatic treatment e.g. phenytoin for seizures

324
Q

Herpes zoster (shingles) pathology

A

Varicella-zoster virus (VZV) is highly contagious and most individuals are infected in childhood, leading to chickenpox.
Transmitted by respiratory droplets
Infection is lifelong due to viral latency within sensory ganglia.
Reactivation of the virus in adulthood leads to herpes zoster (shingles).

325
Q

clinical manifestations of chicken pox

A

Fever
Malaise
Headache
Abdominal pain
Rash: pruritic, erythematous macules -> vesicles, crust

326
Q

clinical manifestations of shingles

A

Presents as a band-like vesicular eruption along the distribution of a sensory nerve. (Macular -> vesicular rash in dermatomal distribution)
Painful, hyperaesthetic area
Infectious until scabs appear

327
Q

investigations for shingles

A

Clinical diagnosis (based on rash within a dermatome) unless immunosuppressed:
Viral PCR, culture, immunofluorescence

328
Q

treatment of shingles

A

Oral acyclovir/ valaciclovir for uncomplicated chicken pox/shingles in adults. Aim to give within 48 hours of rash
IV acyclovir if pregnant, immunosuppressed, severe/disseminated disease

329
Q

prevention of herpes zoster

A

not routine in children in UK, given at aged 70 to prevent shingles reactivation

330
Q
A

Phase 2a Medicine (10 decks)

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