Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

Define headache.

A

Pain in the face, head or neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Acute new headache: what are the three main features of meningitis?

A

Fever, photophobia, stiff neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute new headache: what are the three main features of encephalitis?

A

Fever, confusion, decreased GCS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Acute new headache: what are the main features of subarachnoid haemorrhage?

A

Thunderclap headache, stiff neck, vomiting, fits, confusion, eye pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Acute new headache: what are the main features of head injury?

A

Bruising, decreased GCS, lucid periods, amnesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Acute new headache: what are the main features of self-limiting illness?

A

Sore throat, low grade fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute new headache: what are the main features of sinusitis?

A

Tender of sinuses, history of upper respiratory tract infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute recurrent headache: what are the main features of migraine?

A

Aura, visual + speech changes, nausea + vomiting, numbness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Acute recurrent headache: what are the main features of cluster headache?

A

Intense sharp stabbing eye pain, redness, lid swelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acute recurrent headache: what is the main feature of exertional headache?

A

History of association with activities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute recurrent headache: what are the main features of trigeminal neuralgia?

A

Intense stabbing eye pain, redness, lid swelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Acute recurrent headache: what are the main features of glaucoma?

A

Red eye, halos, decreased visual acuity, pupil abnormality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Subacute headache: what are the main features of giant cell arteritis?

A

Age > 50, scalp tenderness, increased ESR, anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic headache: what are the main features of tension headache?

A

Bilateral tightening, associated with stress + anxiety.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Chronic headache: what are the main features of medication overuse headache?

A

Rebound headaches on stopping analgesia, taking medication for longer than three months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic headache: what are the main features of intracranial hypertension?

A

Non-pulsatile, bilateral, worse in morning, visual changes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give examples of headache red flags.

A

Aged over 50, new onset, vomiting w/o cause, postural differences, eye pain, occurs after trauma, new with hx of cancer, seizures, loss of consciousness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is meningitis?

A

A life-threatening condition of acute inflammation of the meninges.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the meninges?

A

The protective membranes of the brain and spinal cord (dura mater, arachnoid mater, pia mater).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two mechanisms by which meningitis may develop from an infection?

A

Haematogenous spread.

Direct spread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Meningitis: What is haematogenous spread?

A

Pathogen enters the bloodstream and moves through the blood brain barrier.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Meningitis: What is direct spread?

A

Pathogen penetrates CSF due to anatomical defects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Meningitis: describe how cerebral oedema and raised intracranial pressure develop.

A

WBCs identify the pathogen in the blood and the CSF. WBCs release cytokines to recruit more WBCs… the BBB becomes more permeable and more fluid crosses… increasing CSF pressure. Inflammation and endothelial damage = cerebral oedema and raised ICP.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Meningitis: describe how hydrocephalus develops.

A

Fibrin deposits block resorption of CSF by arachnoid villi, causing hydrocephalus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the three types of meningitis?

A

Viral meningitis.
Bacterial meningits.
Non-infectious meningitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Of the three types of meningitis, which is most common?

A

Viral meningitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the three most common causes viral meningitis?

A

Coxsackie (enteroviruses).
Herpes simplex virus.
Varicella zoster virus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the two most common causes of bacterial meningitis in adults?

A

Neisseria meningitidis.

Streptococcus pneumoniae.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the two most common causes of bacterial meningitis in neonates?

A

Group B streptococcus.

E. coli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are non-infectious causes of meningitis?

A

Malignancy.
Autoimmune disease.
Adverse drug reactions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does meningitis present?

A

Fever, headache, photophobia and neck stiffness. As well as confusion and focal neurological deficits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is meningitis investigated?

A

Lumbar puncture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What does lumbar puncture reveal in bacterial meningitis?

A

Raised white cells, polymorphonuclear cells (e.g. neutrophils), low glucose and high protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does lumbar puncture reveal in viral meningitis?

A

Raised white cells, lymphocytes, normal glucose, normal/high protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What does lumbar puncture reveal in tuberculosis meningitis?

A

Raised white cells, lymphocytes, v. low glucose, v. high protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Meningitis: investigation by lumbar puncture is contraindicated under what circumstances?

A

In patients with cardiorespiratory instability or in patients with signs of raised intracranial pressure (vomiting, visual changes, behaviour changes, weakness).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Why is lumbar puncture contraindicated with raised intracranial pressure?

A

Risk of coning the cerebellum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is bacterial meningitis managed in the community?

A

In cases with non-blanching rash give single dose IM/IV benzylpenicillin before immediate transfer to hospital.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is bacterial meningitis managed in the hospital setting?

A

Aged < 3 months: IV cefotaxime + amoxicillin.
Aged ≥ 3 months: IV ceftriaxone.
Give dexamethasone to reduce inflammation and complications.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How is viral meningitis managed?

A

Normally resolves spontaneously, can give aciclovir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Who should receive meningococcal chemoprophylaxis and in what form?

A

Household members should receive ciprofloxacin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the most common complication of bacterial meningitis?

A

Sensorineural hearing loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is encephalitis?

A

Inflammation of the cerebral cortex.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What groups of people does encephalitis typically affect?

A

The immunocompromised.

Those at the extremes of age (e.g. < 1 yr, > 65yrs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is the presentation of acute encephalitis?

A

Fever, confusion, decreased consciousness, headache, seizures and vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the most common cause of acute encephalitis?

A

Herpes simplex virus type-1.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How is acute encephalitis investigated?

A

Lumbar puncture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the results of lumbar puncture in acute encephalitis?

A

Lymphocytosis and elevated protein in the CSF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the management of acute encephalitis?

A

Intravenous acyclovir.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is subarachnoid haemorrhage?

A

Bleeding beneath the arachnoid mater into the cerebrospinal fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the two causes of subarachnoid haemorrhage?

A

Trauma.

Spontaneous development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give examples of possible triggers for spontaneous subarachnoid haemorrhage.

A

Strenuous activity such as weight lifting or sex that can cause an aneurysm to rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the characteristic presenting feature of subarachnoid haemorrhage?

A

Acute severe occipital headache (thunderclap!)… often described as a blow to back of the head.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Other than thunderclap headache, what are the features of subarachnoid haemorrhage?

A

Stiff neck, decreased consciousness, photophobia, vision, changes and focal neurological deficit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Give four risk factors for subarachnoid haemorrhage?

A

Hypertension, smoking, excessive alcohol consumption and cocaine use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the primary imaging investigation in suspected subarachnoid haemorrhage?

A

CT head.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the results of CT head in subarachnoid haemorrhage?

A

Hyperattenuation in the subarachnoid space. Note: negative imaging doesn’t exclude SAH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

SAH: What investigation can be performed if CT head negative but SAH still suspected?

A

Lumbar puncture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are the results of lumbar puncture in subarachnoid haemorrhage?

A

Red blood cells and xanthochromia (bilirubin… breakdown of RBCs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What pharmacological intervention can be provided in subarachnoid haemorrhage?

A

Nimodipine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Management of SAH: explain why nimodipine is given.

A

Nimodipine is a calcium channel blocker which prevents cerebral artery vasospasm (risk of brain ischaemia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What investigation may be performed in subarachnoid haemorrhage prior to neurosurgical intervention?

A

Cerebral angiography for the detection, demonstration and localisation of ruptured aneurysms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the neurosurgical management options of subarachnoid haemorrhage?

A

Neurosurgical clipping.

Endovascular coiling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the Glasgow Coma Scale?

A

A universal assessment tool for assessing the level of consciousness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What three factors contribute to the Glasgow Coma Scale?

A

Eyes, verbal response and motor response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How are eyes scored on the Glasgow Coma Scale?

A

4 - open spontaneously.
3 - open to voice.
2 - open to pain.
1 - no opening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

How is verbal response scored on the Glasgow Coma Scale?

A 
5 - orientated, normal conversation. 
4 - confused conversation. 
3 - inappropriate words. 
2 - incomprehensible sounds. 
1 - no verbal response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How is motor response scored on the Glasgow Coma Scale?

A 
6 - obeys commands. 
5 - localises to pain. 
4 - normal flexion to pain. 
3 - abnormal flexion to pain. 
2 - extends to pain. 
1 - no motor response.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What GCS score indicates that a patient may need their airway securing?

A

8/15 or below.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is chronic subdural haematoma?

A

Collection of blood within the subdural space (between the dural and arachnoid mater).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the clinical features of subdural haemorrhage?

A

Progressive history of confusion, reduced consciousness or neurological deficit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Subdural haemorrhage commonly occurs due to rupture of which vessels?

A

Bridging veins which cross the subdural space.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Which groups of people are more vulnerable to subdural haemorrhage and why?

A

Alcoholics and the elderly. Both have brain atrophy which makes the bridging veins more exposed and vulnerable to rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does CT head reveal in chronic subdural haematoma?

A

Crescentic, hypodense collection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the difference between acute subdural haemorrhage and chronic subdural haematoma on CT head?

A

Blood is hyperdense in acute haemorrhage and hypodense in chronic haematoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Chronic subdural haematoma is defined as existing for how long a period of time?

A

At least three weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

In subdural haemorrhage, why does blood form a crescentic pattern on CT head?

A

Haemorrhage is not limited by suture lines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the management of acute subdural haemorrhage and chronic subdural haematoma?

A

Surgical decompression for both. Acute haemorrhage requires craniotomy while chronic haematoma can be resolved with burr holes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is extradural haemorrhage?

A

Bleeding between the skull and dura (the outermost layer of the meninges).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Extradural haemorrhage most commonly develops as a result of rupture of which vessel?

A

Middle meningeal artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Why is the middle meningeal artery particularly vulnerable to rupture?

A

The middle meningeal artery overlies the pterion, a particularly thin and weak point of the skull (where the temporal, frontal, parietal and sphenoid bones join).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the classic presentation of extradural haemorrhage?

A

Patient loses, briefly regains, then loses consciousness again following a low-impact head injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

How does extradural haemorrhage appear on CT imaging?

A

Biconvex, hyperdense collection around the surface of the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Why do extradural haemorrhages appear as biconvex on CT imaging?

A

The haemorrhage is limited by suture lines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the management of extradural haemorrhage?

A

Craniotomy and surgical evacuation of the haemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Give three possible causes of brain abscess?

A

Extension of sepsis from the middle ear or sinuses.
Penetrating head injuries.
Embolic events from endocarditis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the presentation of a brain abscess?

A

Fever, headache and focal neurology (depending on the site of the abscess).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are focal neurologic signs?

A

Impairments of nerve, spinal cord or brain function that affect a specific region of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are five causes of focal neurologic signs?

A

Head trauma, tumours, stroke, meningitis or encephalitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Frontal lobe signs most commonly involve what system?

A

The motor system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Give examples of frontal lobe signs.

A

Unsteady gait, hypertonia, limb paralysis, expressive aphasia, change in personality, grand mal / tonic-clonic seizures,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Parietal lobe signs most commonly involve what system?

A

Somatosensory system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Give examples of parietal lobe signs.

A

Impairment of tactile sensation and proprioception, sensory/visual neglect, loss of ability to read, write and calculate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Temporal lobe signs most commonly involve what system?

A

Auditory sensation and memory systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Give examples of parietal lobe signs.

A

Cortical deafness, tinnitus, auditory hallucinations, sensory aphasia, amnesia/memory loss, complex partial seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Occipital lobe signs most commonly involve what system?

A

Visual sensation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Give examples of occipital lobe signs.

A

Cortical blindness, visual field impairment, visual agnosia, visual hallucinations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Cerebellar signs most commonly involve what system?

A

Balance and coordination.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Give examples of cerebellar signs.

A

Cerebellar ataxia (broad based gait), intention tremor, dysdiadochokinesia, nystagmus, dysarthria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is a common pathological consequence of brain abscess?

A

Abscesses have a considerable mass effect in the brain and raised intracranial pressure is common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

How are brain abscesses investigated?

A

CT imaging.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

How are brain abscesses managed medically?

A

Intravenous ceftriaxone and metronidazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

How are brain abscesses managed surgically?

A

Craniotomy and debridement of the abscess cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Define migraine.

A

Recurrent, sever headache which is usually unilateral and throbbing in nature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What clinical features are typically associated with migraine?

A

Along with unilateral throbbing headache… aura, nausea and photosensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Migraine: How long can the headache last?

A

4-72 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Migraine: What is aura?

A

Visual changes associated with migraines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Migraine: Give examples of aura.

A

Sparks in vision.
Blurring vision.
Lines across vision.
Loss of different visual fields.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Migraine: How long can aura last?

A

15-60 minutes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Give examples of potential migraine triggers.

A

Chocolate, oral contraceptive, caffeine, alcohol, travel, exercise (chocolate mnemonic). As well as stress, bright lights, dehydration and menstruation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the pharmacological management of acute migraine?

A 
Oral triptan (e.g. sumatriptan) + NSAID. 
//or//
Oral triptan + paracetamol.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is pharmacological prophylaxis for migraine?

A

Topiramate or propranolol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

When should people be offered migraine prophylaxis?

A

Having two attacks of migraine per month.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Migraine management: what effects choice of topiramate v propranolol in migraine prophylaxis?

A

Topiramate should not be given to women of childbearing potential (teratogenic).
Propranolol should be avoided in asthmatics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How is migraine management different in women?

A

Women may find that frequency and severity of migraines increases around menstruation. Treatment with mefenamic acid or a combination of aspirin, paracetamol or caffeine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Describe the pattern by which cluster headaches can occur.

A

Headaches occur once or twice a day in clusters lasting several weeks… with a cluster occurring once a year.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Cluster headaches are more common in which two groups?

A

Men.

Smokers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the characteristic presentation of a cluster headache?

A

Intense, sharp, stabbing pain around one eye.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

How long do episodes of cluster headache last for?

A

15 minutes to 3 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

As well as sharp pain around the eye, what are other features of cluster headaches?

A

Redness, miosis, ptosis, lacrimation, eyelid swelling and nasal congestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How are cluster headaches managed acutely?

A

100% oxygen via a non-rebreathe mask with 6mg subcutaneous sumatriptan.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What short-term prevention regimens can be used in the management of cluster headaches?

A

Oral prednisolone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What longer-term prevention regimens can be used in the management of cluster headaches?

A

Oral verapamil.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Give three examples of potential triggers of cluster headache?

A

Alcohol.
Exercise.
Strong smells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

How are cluster headaches investigated?

A

MRI to exclude secondary causes e.g. tumours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is trigeminal neuralgia?

A

Syndrome characterised by severe unilateral facial pain along the branches of the trigeminal nerve (ophthalmic, maxillary, mandibular).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the clinical presentation of trigeminal neuralgia?

A

Brief, unilateral, electric shock-like pains that are abrupt in onset and termination. Pain is commonly evoked by light touch (washing, shaving, talking).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the causes of trigeminal neuralgia?

A

Idiopathic.
Compression of nerve roots by tumours.
Vascular problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the first-line pharmacological management of trigeminal neuralgia?

A

Carbamazepine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What is temporal arteritis?

A

A large vessel vasculitis that commonly presents with unilateral headache.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is the clinical presentation of temporal arteritis?

A

Unilateral headache, jaw claudication, visual disturbances, tender + palpable temporal artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the result of investigations in temporal arteritis?

A

Raised inflammatory markers.

Skip lesions present on biopsy of the temporal artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the treatment of temporal arteritis?

A

High-dose prednisolone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Describe the features of tension headache.

A

Recurrent, non-disabling, bilateral headache often described as a tight-band.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is the management of tension headaches?

A

Advise yoga, meditation and exercise to try to alleviate stress and anxiety. If necessary provide simple analgesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Define raised intracranial pressure and what is normal intracranial pressure?

A

Pressure exerted inside the skull is increased (normal intracranial pressure is 7-15 mmHg in the supine position).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are five potential causes of raised intracranial pressure?

A

Idiopathic intracranial hypertension, traumatic head injuries, infection, tumours and hydrocephalus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How does raised intracranial pressure present clinically?

A

Headache (non-pulsatile, bilateral, worse in mornings), vomiting, reduced consciousness, visual disturbance (including transient visual darkening).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Raised ICP: What is Cushing’s triad?

A

Signs indicative of raised ICP: widened pulse pressure, bradycardia and irregular respirations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Raised ICP: What does investigation with fundoscopy reveal?

A

Bilateral papilloedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How is raised ICP treated?

A

Intravenous mannitol or CSF removal via shunt or repeated lumbar puncture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Idiopathic intracranial hypertension typically affects what group of people?

A

Young, obese women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What is spontaneous intracranial hypotension?

A

A rare cause of hypotension that develops due to a low level of CSF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is the clinical presentation of spontaneous intracranial hypotension?

A

Headache worse on standing and improves when lying flat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What is tuberous sclerosis?

A

Genetic condition that involves the growth of hamartomas (benign neoplastic growth of the tissue that they originate from) on the brain and other organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What are neurocutaneous features of tuberous sclerosis?

A

Ash leaf spots (depigmented areas of skin). Roughened patches of skin over lumbar spine. Angiofibromas (papules across nose and cheeks). Fibromata beneath nails. Poliosis (isolated patch of white hair).

147
Q

What are neurological features of tuberous sclerosis?

A

Epilepsy.

Learning disability with developmental delay.

148
Q

What is neurofibromatosis?

A

Group of conditions characterised by benign tumours that grow in the nervous system (neuromas).

149
Q

What are the two types of neurofibromatosis and which is most common?

A

Neurofibromatosis type 1 (more common).

Neurofibromatosis type 2.

150
Q

What chromosome is the neurofibromatosis type 1 gene found on?

A

Chromosome 17.

151
Q

Neurofibromatosis type 1 gene codes for what protein?

A

Neurofibromin (a tumour suppressor protein).

152
Q

What is the inheritance pattern of mutations to the neurofibromatosis type 1 gene?

A

Autosomal dominant.

153
Q

What are the diagnostic criteria of neurofibromatosis type 1?

A

C – café-au-lait spots.
R – relative with NF1.
A – axillary/inguinal freckles.
BB – bony dysplasia e.g. bowing of a long bone.
I – iris hamartomas (yellow/brown spots on the iris).
N – neurofibromas (2 or more).
G – glioma of the optic nerve.

154
Q

What chromosome is the neurofibromatosis type 2 gene found on?

A

Chromosome 22.

155
Q

Neurofibromatosis type 2 gene codes for what protein?

A

Merlin (a tumour suppressor protein important in Schwann cells).

156
Q

What is the inheritance pattern of mutations to the neurofibromatosis type 2 gene?

A

Autosomal dominant.

157
Q

What is the most common type of schwannoma that develops in neurofibromatosis type 2?

A

Acoustic neuroma.

158
Q

Neurofibromatosis type 2: What are the clinical features of acoustic neuromas?

A

Hearing loss, tinnitus and balance problems.

159
Q

Define transient ischaemic attack (TIA).

A

Transient episode of neurological dysfunction cause by focal brain, spinal cord or retinal ischaemia without acute infarction.

160
Q

What is 14-day risk of stroke following TIA? (%)

A

10%.

161
Q

What is the management of transient ischaemic attack?

A

300mg aspirin.

Clopidogrel for three months.

162
Q

Define stroke.

A

Sudden interruption in the vascular supply of the brain that causes neuronal death and thus irreversible damage.

163
Q

What are the two main types of stroke?

A 
Ischaemic stroke (majority). 
Haemorrhagic stroke.
164
Q

What are clinical features of stroke?

A

Motor weakness, dysphasia, swallowing problems, visual field defects and balance problems.

165
Q

Total anterior circulation infarcts involve which vessels?

A

Middle and anterior cerebral arteries.

166
Q

Total anterior circulation infarcts present with which three features?

A

Unilateral hemiparesis and/or hemisensory loss of face, arm and leg.
Homonymous hemianopia.
Higher cognitive dysfunction (dysphagia).

167
Q

Partial anterior circulation infarcts involve which vessels?

A

Smaller arteries of anterior circulation (upper/lower division of middle cerebral arteries).

168
Q

Partial anterior circulation infarcts present with two of which three features?

A

Unilateral hemiparesis and/or hemisensory loss of face, arm and leg.
Homonymous hemianopia.
Higher cognitive dysfunction (dysphagia).

169
Q

Lacunar infarcts involve which vessels?

A

Penetrating arteries around the internal capsule, thalamus, basal ganglia.

170
Q

Lacunar infarcts present with one of which three features?

A

Unilateral weakness of face + arm, arm + leg or all three.
Pure sensory stroke.
Ataxic hemiparesis.

171
Q

Posterior infarcts involve which vessels?

A

Vertebrobasilar arteries.

172
Q

Posterior infarcts present with one of which three features?

A

Cerebellar or brainstem syndromes.
Loss of consciousness.
Isolate homonymous hemianopia.

173
Q

Suspected strokes require which urgent investigation and why?

A

CT or MRI head to classify strokes into ischaemic or haemorrhagic.

174
Q

What is the management of ischaemic strokes which present within 4.5 hours of symptom onset?

A

Intravenous alteplase (thrombolytic therapy).

175
Q

What are contraindications for alteplase use in the management of ischaemic stroke?

A

Previous intracranial haemorrhage, seizure at onset of stroke, intracranial neoplasm, pregnancy, preceding gastrointestinal bleeding and active bleeding.

176
Q

What is the management of ischaemic strokes which aren’t suitable for thrombolytic therapy but present within 24 hours of symptom onset?

A

Mechanical thrombectomy.

177
Q

What is provided for secondary prevention of ischaemic strokes?

A

75mg clopidogrel.

178
Q

What structural disease can increase the risk of an ischaemic stroke?

A

Carotid artery stenosis.

179
Q

How is carotid artery stenosis investigated?

A

Duplex ultrasound followed by CT angiography.

180
Q

What is the management of carotid artery stenosis?

A

Carotid artery endarterectomy or stenting.

181
Q

What are two causes of haemorrhagic stroke (and which is most common)?

A

Hypertension (most common).

Amyloid angiopathy.

182
Q

Where do haemorrhagic strokes secondary to hypertension most commonly occur?

A

Cerebellum, thalamus and/or basal ganglia.

183
Q

Describe the pathophysiology behind amyloid angiopathy and the development of haemorrhagic strokes?

A

Amyloid angiopathy is characterised by protein deposition which increases vascular fragility and thus the risk of rupture… bleeding.

184
Q

Where do haemorrhagic strokes secondary to amyloid angiopathy most commonly occur?

A

Cerebral cortex.

185
Q

What is the management of haemorrhagic stroke?

A

Stop anticoagulation and reverse (if applicable).
Control hypertension with labetalol (aim for SBP < 140).
If amenable refer to neurosurgery for craniotomy.

186
Q

How is anticoagulation by warfarin reversed?

A

Give dried prothrombin complex (beriplex) and vitamin K (phytomenadione).

187
Q

What is a facial nerve palsy?

A

Isolated dysfunction of the facial nerve and weakness of structures it supplies.

188
Q

What are the functions of the facial nerve?

A

Motor: muscles of facial expression and stapedius muscle. Sensory: taste sensation from the anterior 2/3 of the tongue. Parasympathetic: salivary and lacrimal glands.

189
Q

How is an upper motor neurone and lower motor neurone facial nerve palsy differentiated?

A

Upper motor neurone lesions spare the upper face (forehead) whereas lower motor neurone lesions affect all facial muscles.

190
Q

Give examples of a cause of an upper motor neurone lesion and lower motor neurones facial nerve palsy?

A

Upper - stroke.

Lower - Bell’s palsy.

191
Q

What is Bell’s palsy?

A

Acute, unilateral, idiopathic, facial nerve paralysis.

192
Q

How does Bell’s palsy present clinically?

A

Lower motor neurone facial nerve palsy affecting all facial muscles (including forehead). Post-auricular pain, altered taste, dry eyes and hyperacusis.

193
Q

What is the management of Bell’s palsy?

A

10 day course of prednisolone given within 72 hours of onset.

194
Q

What is the prognosis of Bell’s palsy if left untreated?

A

15% of untreated patients will develop permanent moderate-to-severe weakness. The rest resolve.

195
Q

What is a third nerve palsy?

A

Eye condition resulting from damage to the oculomotor nerve (or a branch thereof).

196
Q

What is the function of the oculomotor nerve?

A

Supplies a majority of muscles controlling eye movement EXCEPT lateral rectus and superior oblique.

197
Q

How does a third nerve palsy present clinically?

A

‘Down and out’ eye deviation and ptosis.

198
Q

A defect to the left oculomotor nerve affects which eye (right or left)?

A

Left - cranial nerves don’t cross sides (except CNIV)

199
Q

What is a surgical third nerve palsy?

A

Third nerve palsy (down and out) + dilated pupil with absent light reflex.

200
Q

What is the management of a surgical third nerve palsy?

A

Requires urgent brain imaging to exclude bleed/aneurysm.

201
Q

What is epilepsy?

A

A condition characterised by recurrent seizures.

202
Q

How is epilepsy classified?

A

Depending on where the seizure begins in the brain, the level of awareness of the individual during the seizure, motor, non-motor and other features.

203
Q

What are the main clinical features of epilepsy?

A

Loss of consciousness, limb jerking, tongue biting and incontinence.

204
Q

What are the two main groups of seizure?

A

Generalised.

Focal.

205
Q

What is the difference between generalised and focal seizures?

A

Generalised seizures result in loss of consciousness whereas focal seizures result in varying consciousness.

206
Q

What is the first-line treatment of generalised seizures?

A

Sodium valproate (avoid in females of childbearing potential).

207
Q

What is the first-line treatment of focal seizures?

A

Carbamazepine.

208
Q

What is a common second-line option in treatment of epilepsy?

A

Lamotrigine.

209
Q

Epilepsy: What typically follows seizure?

A

Postictal period (drowsy and tired) for around fifteen minutes.

210
Q

Following an epileptic seizure and EEG / brain imaging is normal… how long must a patient not drive for?

A

Six months.

211
Q

Following an epileptic seizure and EEG / brain imaging is abnormal… how long must a patient not drive for?

A

Twelve months.

212
Q

What are the typical features of a generalised tonic-clonic seizure?

A

Loss of consciousness, stiffening, body jerking.

213
Q

What are the typical features of a temporal lobe (focal) seizure?

A

Plucking clothes, lip smacking, aura, deja-vu.

214
Q

What are the typical features of a frontal lobe (focal) seizure?

A

Motor abnormalities and Jacksonian movements.

215
Q

What are the typical features of a parietal lobe (focal) seizure?

A

Sensory abnormalities (tingling, numbness).

216
Q

What are the typical features of juvenile myoclonic epilepsy?

A

Absence, myoclonus, tonic-clonic seizure.

217
Q

What are absence seizures?

A

Form of generalised epilepsy mostly seen in children.

218
Q

How do absence seizures present?

A

Absence/vacant lasting for a few seconds followed by quick recovery.

219
Q

What does EEG reveal in absence seizures?

A

Bilateral, symmetrical 3Hz spike and wave pattern.

220
Q

What is the management and prognosis of absence seizures?

A

Manage with sodium valproate / ethosuximide. Most become seizure-free in adolescence.

221
Q

What are psychogenic non-epileptic seizures?

A

Pseudoseizures. Events resemble epileptic seizures but lack the characteristic electrical discharges associated with epilepsy.

222
Q

What are features of psychogenic non-epileptic seizures?

A

Gradual onset with pelvic thrusting. Crying post-seizure.

223
Q

What investigation can be used to differentiate pseudoseizures from true epilepsy?

A

Serum prolactin - prolactin raised 10-20 minutes following true epilepsy (but not pseudoseizure).

224
Q

What is status epilepticus?

A

Seizures lasting longer than five minutes.

225
Q

Why is status epilepticus dangerous?

A

Prolonged seizures = hypoxia = irreversible brain damage.

226
Q

What is the treatment of status epilepticus in hospital?

A

Intravenous lorazepam.

227
Q

Status epilepticus: How soon can intravenous lorazepam be repeated?

A

Repeated once after 10 minutes.

228
Q

Status epilepticus: if seizures don’t resolve after two doses of lorazepam, what treatment should be given?

A

Intravenous phenytoin.

229
Q

What is the treatment of status epilepticus in the prehospital setting?

A

Buccal midazolam or rectal diazepam.

230
Q

What is dementia?

A

A syndrome encompassing progressive deficits across several cognitive domains.

231
Q

Give four causes of dementia.

A

Alzheimer’s disease.
Vascular dementia.
Lewi-body dementia.
Fronto-temporal dementia.

232
Q

How does dementia present?

A

Memory loss over months or years. Non-cognitive symptoms include agitation, aggression or apathy.

233
Q

Give examples of two assessment tools used in the diagnosis of dementia.

A

10-point cognitive screener (10-CS).

6-item cognitive impairment test (6CIT).

234
Q

What are two differential diagnoses to dementia of memory loss over hours/days?

A

Infection.

Stroke.

235
Q

What are differential diagnoses to dementia of memory loss over several weeks?

A

Depression.
Hypothyroidism.
B12/folate/thiamine deficiency.

236
Q

What investigations are performed for dementia in primary care?

A

Confusion screen (FBC, U&Es, LFTs, calcium, glucose, TFTs, vitamin B12, folate).

237
Q

In the diagnosis of dementia, neuroimaging is important in the exclusion of which conditions?

A

Subdural haematoma.

Normal pressure hydrocephalus.

238
Q

Give examples of social support that can be provided to dementia patients.

A 
Laundry services. 
District nurses. 
Attendance allowance. 
Respite care in hospital. 
Day care and lunch clubs. 
Council tax rebate.
239
Q

What is the most common cause of dementia?

A

Alzheimer’s disease.

240
Q

What is the presentation of Alzheimer’s dementia?

A

Enduring, progressive and global cognitive impairment.

241
Q

Describe the pathophysiology of Alzheimer’s dementia.

A

Accumulation of beta-amyloid peptide (degradation product of amyloid precursor) results in progressive neuronal damage, neurofibrillary tangles and increased numbers of amyloid plaques.

242
Q

What are the clinical features of Alzheimer’s dementia?

A

Impairment of visuo-spatial skill (gets lost), memory, verbal abilities and executive function (planning).

243
Q

What are later clinical features of Alzheimer’s dementia?

A

Irritability, mood disturbance and behavioural change (wandering, aggression, disinhibition).

244
Q

What pharmacological intervention can be considered first-line in Alzheimer’s dementia?

A

Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine).

245
Q

What pharmacological intervention can be considered second-line in Alzheimer’s dementia?

A

Memantine (NMDA receptor antagonist).

246
Q

What is vascular dementia?

A

The cumulative effect of many small strokes.

247
Q

How does vascular dementia present?

A

Sudden onset, stepwise deterioration of cognitive impairment.

248
Q

What are the clinical features of vascular dementia?

A

Focal neurological abnormalities, attention/concentration difficulty, seizures, memory disturbance and gait/speech/emotional disturbance.

249
Q

What is Lewy-body dementia?

A

Dementia characterised by alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

250
Q

What are the clinical features of Lewy-body dementia?

A

Fluctuating cognitive impairment, Parkinsonism and hallucinations.

251
Q

What is fronto-temporal dementia?

A

A type of cortical dementia characterised by frontal and temporal atrophy without Alzheimer histology.

252
Q

What is the presentation of fronto-temporal dementia?

A

Insidious onset typically before the age of 65 years with personality change and social conduct problems.

253
Q

What is Pick’s dementia?

A

The most common subtype of fronto-temporal dementia.

254
Q

What are the clinical features of Pick’s dementia?

A

Personality change, impaired social conduct, hyperorality, disinhibition, increased appetite and preservation behaviour.

255
Q

What is normal pressure hydrocephalus?

A

Reversible cause of dementia caused by reduced CSF absorption at the arachnoid villi (secondary to head injury, subarachnoid haemorrhage and meningitis).

256
Q

What is the classic triad of features of normal pressure hydrocephalus?

A

Urinary incontinence, gait abnormality and dementia (wet, wobbly and wacky).

257
Q

What investigation is performed in normal pressure hydrocephalus and what are the results?

A

Neurological imaging (CT or MRI). Hydrocephalus with ventriculomegaly.

258
Q

How should normal pressure hydrocephalus be managed?

A

Ventriculoperitoneal shunting.

259
Q

What is benign essential tremor?

A

Neurological disorder that causes involuntary and rhythmic shaking in voluntary muscles.

260
Q

What are clinical features of essential tremor?

A

Fine tremor of the hands, head and jaw. Pt may also have a vocal tremor.

261
Q

What is the management of essential tremor?

A

Rest typically improves symptoms. Pharmacological management includes propranolol (beta-blocker).

262
Q

What is Guillain-Barre syndrome?

A

Syndrome of rapid-onset muscle weakness as a result of autoimmune damage to the peripheral nervous system.

263
Q

What is the most common pathophysiological process behind the development of Guillain-Barre syndrome?

A

Acute inflammatory demyelinating neuropathy

264
Q

Describe the process behind the acute inflammatory demyelinating neuropathy in Guillain-Barre syndrome?

A

White blood cells produce antibodies against the preceding infection which inappropriately match with proteins on the myelin sheath… causing damage.

265
Q

Two thirds of cases of Guillain-Barre syndrome are preceded by what?

A

Gastrointestinal or upper respiratory tract infections.

266
Q

When does Guillain-Barre syndrome typically develop post gastrointestinal / upper respiratory tract infection?

A

Four weeks.

267
Q

What are the most common bacterial pathogens that precede Guillain-Barre syndrome?

A

Campylobacter jejuni.

Mycoplasma pneumoniae.

268
Q

What are the two most common viral pathogens that precede Guillain-Barre syndrome?

A

Cytomegalovirus.

Epstein-Barr virus.

269
Q

What is the characteristic presentation of Guillain-Barre syndrome?

A

Progressive ascending weakness (starting in the hands and feet) with/without paraesthesia.

270
Q

What are the potential clinical features of Guillain-Barre syndrome (other than weakness)?

A

Loss of sensation, absence of reflexes, cranial nerve involvement (double vision, dysarthria, difficulty swallowing), autonomic dysfunction (blood pressure irregularity, constipation, urinary incontinence).

271
Q

How is diagnosis of Guillain-Barre syndrome made?

A

Clinically with supportive investigations (nerve conduction studies and CSF analysis).

272
Q

What do nerve conduction studies reveal in Guillain-Barre syndrome?

A

Focal conduction block is characteristic of GBS.

273
Q

What does CSF analysis reveal in Guillain-Barre syndrome?

A

Elevated protein.

274
Q

How is Guillain-Barre syndrome treated?

A

Give intravenous immunoglobulin to neutralise harmful antibodies. If no response perform plasmapheresis. Give VTE prophylaxis (LMWH).

275
Q

How should neuropathic pain be managed in Guillain-Barre syndrome?

A

Mod-severe pain give tramadol.

276
Q

How should individuals with Guillain-Barre be monitored for life-threatening complications?

A

Respiratory muscles may be affected - four-hourly monitoring of forced vital capacity is essential in anticipating respiratory failure. FVC < 20mL/kg warrants transfer to ICU for potential intubation and ventilation.

277
Q

What is Miller-Fisher syndrome?

A

A variant of Guillain-Barre syndrome that presents as a descending paralysis (causing ophthalmoplegia, ataxia and areflexia).

278
Q

What is Huntington’s disease?

A

An incurable progressive neurodegenerative condition.

279
Q

What is the inheritance pattern of Huntington’s disease?

A

Autosomal dominant.

280
Q

What type of mutation results in the development of Huntington’s disease?

A

Trinucleotide repeat disorder - mutation in the huntingtin (HTT) gene on chromosome 4.

281
Q

Huntington’s disease: Trinucleotide repeat disorders are characterised by what genetic phenomenon?

A

Genetic anticipation.

282
Q

Huntington’s disease: Explain genetic anticipation.

A

The disease presents at an earlier age with increased severity in successive generations.

283
Q

Features of Huntington’s disease typically develop at what age?

A

After 35 years.

284
Q

How does Huntington’s disease present initially?

A

Personality changes (irritability, apathy, depression) and intellectual impairment.

285
Q

Huntington’s disease: Following the development of personality changes, how does the disease progress?

A

Development of chorea (jerky body movements), dystonia and saccadic eye movements.

286
Q

How is Huntington’s disease diagnosed?

A

Genetic testing.

287
Q

How is Huntington’s disease managed?

A

No cure. Antipsychotics (olanzapine) and benzodiazepines (diazepam) can be given to suppress disordered movements.

288
Q

What is the prognosis of Huntington’s disease?

A

Life expectancy is 15-20 years following diagnosis. Most common cause of death is pneumonia.

289
Q

What is Parkinson’s disease?

A

A progressive neurodegenerative condition caused by degeneration of dopaminergic neurones in the substantia nigra.

290
Q

What is the mean age of diagnosis of Parkinson’s disease?

A

65 years.

291
Q

Parkinson’s disease: Describe the physiology of the basal ganglia.

A

The basal ganglia normally exert a constant inhibitory influence on a wide range of motor symptoms, preventing them from becoming active at inappropriate times.

292
Q

Parkinson’s disease: Describe the function of dopamine in normal physiology.

A

Dopamine facilitates a reduction in inhibition when a decision is made to perform an action.

293
Q

Describe the pathophysiology of Parkinson’s disease.

A

Death of dopaminergic neurones leads to lower levels of dopamine in the striatum and thus greater exertion of effort demanded for any given movement.

294
Q

Where is dopamine produced?

A

Substantia nigra pars compacta.

295
Q

What are the three characteristic features of Parkinson’s disease?

A

Bradykinesia, tremor and cogwheel rigidity.

296
Q

Describe the tremor associated with Parkinson’s disease.

A

Asymmetrical resting tremor.

297
Q

Other than the three main features of Parkinson’s disease… how else may the condition present?

A

Mask-like facies.

Postural instability.

298
Q

How is Parkinson’s disease treated?

A

Levodopa.

299
Q

What is levodopa?

A

Dopamine precursor used in the management of Parkinson’s disease.

300
Q

Levodopa is typically combined with what to increase its effectivity?

A

Decarboxylase inhibitor (e.g. carbidopa).

301
Q

Why is co-careldopa (levodopa + carbidopa) more effective than levodopa alone?

A

Carbidopa prevents the peripheral metabolism of levodopa to dopamine.

302
Q

Give examples of side effects of levodopa.

A

Dyskinesia, dry mouth, anorexia, palpitations, postural hypotension, psychosis and drowsiness.

303
Q

What is Parkinson’s disease dementia?

A

Dementia presents in the later stages of Parkinson’s (at least one year of parkinsonian symptoms).

304
Q

What are the features of drug-induced Parkinsonism?

A

Rapid-onset, bilateral motor symptoms while rigidity and resting tremor are uncommon.

305
Q

What is multiple system atrophy?

A

A Parkinsonian-plus syndrome characterised by Parkinsonism with autonomic, corticospinal and cerebellar dysfunction.

306
Q

What are the features of multiple system atrophy?

A

Bradykinesia and cogwheel rigidity with urinary urgency, constipation and postural hypotension.

307
Q

How does the parkinsonian features of multiple system atrophy differ from Parkinson’s disease?

A

MSA does not typically involve resting tremor. Note that in MSA the features are typically symmetrical (as opposed to asymmetrical in Parkinson’s).

308
Q

How is multiple system atrophy treated?

A

Levodopa.

309
Q

What is motor neurone disease?

A

Motor neurone disease is a progressive neurological condition of unknown caused characterised by degenerative of motor neurones in the brain, brain stem and spinal cord.

310
Q

Give examples of patterns of motor neurone disease.

A

Amyotrophic lateral sclerosis.
Progressive bulbar palsy.
Progressive muscular atrophy.

311
Q

What is the most common pattern of motor neurone disease?

A

Amyotrophic lateral sclerosis (AML).

312
Q

What group of people are most commonly affected by motor neurone disease?

A

Late-middle aged men.

313
Q

Amyotrophic lateral sclerosis is characterised by what features?

A

Lower motor neurone signs in the arms and upper motor neurone signs in the legs.

314
Q

What is the clinical presentation of motor neurone disease?

A

Insidious progressive weakness of muscles of limbs, trunk, face and speech. Features include stumbling, foot drop, weakened grip, slurred speech, cramp, muscle wasting, twitching and fatigue.

315
Q

How is diagnosis of motor neurone disease made?

A

Clinical diagnosis with nerve conduction studies to exclude neuropathies.

316
Q

Motor neurone disease: give examples of lower motor neurone signs.

A

Muscle wasting, reduced tone, fasciculations and reduced reflexes.

317
Q

Motor neurone disease: give examples of upper motor neurone signs.

A

Increased tone/spasticity, brisk reflexes and upgoing plantars.

318
Q

What is the management of motor neurone disease?

A

Riluzole may prolong life for up to three months. Be honest with patients about progression, provide analgesia and respiratory care.

319
Q

Explain how riluzole prolongs life in people with motor neurone disease.

A

Riluzole prevents the stimulation of glutamate receptors (excessive stimulation is thought to play a role in the destruction of motor neurones).

320
Q

What is Brown-Sequard syndrome?

A

Condition that results from hemisection of the spinal cause.

321
Q

Give examples of causes of Brown-Sequard syndrome.

A

Tumour, trauma, ischaemia and infectious/inflammatory diseases.

322
Q

Brown-Sequard: What are the clinical features of a corticospinal tract lesion?

A

Ipsilateral weakness below the lesion.

323
Q

Brown-Sequard: What are the clinical features of a dorsal column lesion?

A

Ipsilateral loss of proprioception and vibration sensation.

324
Q

Brown-Sequard: What are the clinical features of a spinothalamic tract lesion?

A

Contralateral loss of pain and temperature sensation.

325
Q

How is Brown-Sequard syndrome investigated?

A

MRI.

326
Q

What is syringomyelia?

A

A collection of CSF fluid within the spinal cord due to anatomical abnormalities… can expand over time to destroy the spinal cord.

327
Q

Give examples of causes of syringomyelia.

A

Chiari malformations, intramedullary tumours, trauma.

328
Q

What is the clinical presentation of syringomyelia?

A

Cough, lower motor neurone weakness in hands and arms, upgoing plantars and dissociate sensory loss affecting spinothalamic sensation (temperature and pain)… patients may accidentally burn their hands without realising.

329
Q

What is multiple sclerosis?

A

An inflammatory demyelinating disease of neurones in the central nervous system (the immune system attacks and destroys myelin).

330
Q

What type of hypersensitivity reaction is multiple sclerosis?

A

Type 4 (cell-mediated) hypersensitivity reaction.

331
Q

Describe the pathophysiology of multiple sclerosis.

A

T lymphocytes bypass the blood-brain barrier and identify myelin-producing oligodendrocytes as foreign. T cells release cytokines which recruit more T cells as well as B cells and macrophages. B cells produce antibodies which mark the myelin sheath and macrophages attack oligodendrocytes - leading to demyelination.

332
Q

What are the four types of multiple sclerosis?

A

Relaxing-remitting multiple sclerosis (RRMS).
Secondary progressive multiple sclerosis (SPMS).
Primary progressive multiple sclerosis (PPMS).
Progressive-relapsing multiple sclerosis (PRMS).

333
Q

What is the most common type of multiple sclerosis?

A

Relapsing-remitting multiple sclerosis (RRMS).

334
Q

Describe the disease course of releasing-remitting multiple sclerosis.

A

Bouts of autoimmune attacks months/years apart which cause increasing disability… there will be some improvement in symptoms initially (remitting) but overtime symptoms will resolve incompletely leaving residual disability.

335
Q

Describe the disease course of secondary progressive multiple sclerosis.

A

Initially similar to RRMS until eventually the immune attack becomes constant causing a steep progression in disability.

336
Q

Describe the disease course of primary progressive multiple sclerosis.

A

A constant attack causing steady progression of disease.

337
Q

Describe the disease course of progressive-relapsing multiple sclerosis.

A

A constant attack as well as superimposed bouts of disease.

338
Q

At what age does multiple sclerosis typically present?

A

20-40 year old.

339
Q

What is the most common presentation of multiple sclerosis?

A

Unilateral optic neuritis (pain on eye movement and rapid decrease in central vision).

340
Q

How may multiple sclerosis present (other than optic neuritis)?

A 
Brainstem or cerebellar symptoms (diplopia, ataxia, nystagmus, intention tremor). 
Sensory symptoms (numbness or tingling in limbs). 
Spastic weakness.
341
Q

How is a diagnosis of multiple sclerosis made (what criteria are used)?

A

Clinically and guided by the McDonald criteria.

342
Q

Multiple sclerosis: What are the McDonald criteria?

A

Multiple lesions in the CNS disseminated in space and time and causes symptoms that last longer than 24 hours.

343
Q

What investigations are used in the diagnosis of multiple sclerosis?

A

MRI.

CSF analysis.

344
Q

Multiple sclerosis: What do MRI and CSF analysis reveal?

A

MRI - white matter plaques.

CSF - oligoclonal bands.

345
Q

What is the treatment of an acute relapse of multiple sclerosis?

A

Corticosteroids (methylprednisolone) - three day high dose intravenous, or five day oral.

346
Q

What is the treatment for long-term remission of multiple sclerosis?

A

Biological agents / disease-modifying drugs.

347
Q

Multiple sclerosis: What treatment is provided for spasticity?

A

Gabapentin or baclofen.

348
Q

What are characteristic features of cauda equina syndrome?

A

Lower back pain, urinary incontinence/retention, reduced sensation to the perianal area and decreased anal tone.

349
Q

What is myasthenia gravis?

A

A long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness.

350
Q

What type of hypersensitivity reaction is myasthenia gravis?

A

Type 2 (antibody-mediated) hypersensitivity reaction.

351
Q

Describe the pathophysiology of myasthenia gravis.

A

B-cells produce antibodies against post-synaptic nicotinic acetylcholine receptors at the neuromuscular junction leading to depletion of these receptors (normal action potentials cannot be generated).
Autoantibodies may also target muscle-specific receptor tyrosine kinase (MuSK) protein.

352
Q

What are the clinical features of myasthenia gravis?

A

Fluctuating muscle weakness and fatiguability. Patients become progressively weaker over the course of a day.

353
Q

What is the most common presenting feature of myasthenia gravis?

A

Vision impairment (ptosis, diplopia) due to extra ocular muscle groups being affected.

354
Q

Myasthenia gravis: Give examples of affected muscle groups and the corresponding features.

A

Extraocular - ptosis, diplopia.
Bulbar - swallowing difficulty, dysarthria.
Face - facial weakness, facial expression loss.
Neck - cannot keep head up.
Limbs - proximal asymmetric muscle weakness.
Respiratory - respiratory failure.

355
Q

20% of cases of myasthenia gravis are associated with what tumour?

A

Thymoma

356
Q

What clinical features are associated with myasthenia w/ thymoma?

A

Cough, shortness of breath.

357
Q

What investigations are performed in myasthenia gravis Gravis?

A 
Antibody testing (acetylcholine receptor antobides and muscle-specific tyrosine kinase). 
Nerve conduction studies.
358
Q

What does antibody testing reveal in myasthenia?

A

Raised AChR-Abs.

Raised MuSK.

359
Q

What do nerve conduction studies reveal in myasthenia?

A

Repetitive stimulation results in progressive decline in muscle action potential.

360
Q

How is myasthenia gravis treated?

A

Pyridostigmine (acetylcholinesterase inhibitor).

High dose prednisolone during relapse.

361
Q

How does pyridostigmine treat myasthenia gravis?

A

Acetylcholinesterase inhibitor prevents the degradation of acetylcholine to increase the concentration of acetylcholine in the synaptic cleft to enhance neuromuscular transmission.

362
Q

What is the primary life-threatening complication of myasthenia gravis?

A

Myasthenic crisis (decrease in function of respiratory muscles).

363
Q

How are people with myasthenia monitored for the development of myasthenic crisis?

A

Regular forced vital capacity (FVC) measurements.

Finals (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions