Brainscape's Knowledge GenomeTM

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


See full index

Phase 2a Sheffield Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a TIA?

A

A transient ischaemic attack (TIA) is a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. It usually resolves spontaneously within 24 hours.

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

What are the risk factors for TIA?

A
  • Increasing age
  • Hypertension
  • Smoking
  • Obesity
  • Diabetes
  • Hypercholesterolaemia
  • Atrial fibrillation
  • Carotid stenosis
  • Thrombophilia disorders e.g. antiphospholipid syndrome
  • Sickle cell disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the signs for TIA?

A
  • Focal neurology: on examination
  • Irregular pulse: suggests atrial fibrillation as an underlying cause
  • Carotid bruit: suggests carotid artery stenosis
  • Hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the symptoms of TIA?

A
  • Contralateral sensory/ motor deficits
  • Facial weakness
  • Limb weakness
  • Dysphasia: slurred speech
  • Ataxia, vertigo, or incoordination
  • Homonymous hemianopia: visual field loss on the same side of both eyes
  • Amaurosis fugax: a painless temporary loss of vision, usually in one eye
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the investigations of a TIA?

A
  • FAST test (Face, Arm, Speech, Time)
  • ECG
  • Auscultation: listen for cartoid bruit
  • Bloods
    • FBC
    • Platelet count
  • Hb1Ac
  • Serum electrolytes
  • Fasting lipid profile
  • ABCD2 - risk stratifying too; for risk of future stroke
  • CT - not until seen by the TIA clinic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the acute management of a TIA?

A
  • Antiplatelet:initiallyaspirin 300mg - FIRST LINE
  • Clopidogrel if allergic
  • Carotid endarterectomy - stenosis of > 70% on Doppler is an indication for urgent endarterectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the secondary prevention management for a TIA?

A
  • Clopidogrel 75mg daily - FIRST LINE
  • Aspirin or subsequently dipyridamole alone as combination is contraindicated.
  • High dose statin - Atorvastatin
  • Manage hypertension, diabetes, smoking, other cardiovascular risk factors
  • Lifestyle advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the complications of TIA?

A
  • Stroke
  • Myocardial infarction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the driving rules around a stroke?

A
  • Car or motorcycle(type 1 license):
    • Patients must not drive for1 monthafter a TIA or stroke
    • Driving may resume after 1 month if there has beensatisfactory clinical recovery
    • Patientsmay not need toinform the DVLA if there is no residual neurological deficit beyond 1 month
    • Multiple TIAsover a short period requires no driving for 3 months
  • Heavy goods vehicle(type 2 license):
    • Patients must not drive for1 yearafter a TIA or stroke
    • Relicensing may be considered after 1 year if there isno significant residual neurologicalimpairment andno other significant risk factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a stroke?

A
  • Stroke is defined as an acute neurological deficit lasting more than 24 hours and caused by cerebrovascular aetiology.
  • It is also referred to as a cerebrovascular accident
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an ischemic stroke? what are the types?

A
  • Reduction in cerebral blood flow due to arterial occlusion or stenosis. Typically divided into lacunar (affecting blood flow in small arteries), thrombotic and embolic
  • Cardiac, vascular, haematological
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is a haemorrhagic stroke? what are the types?

A
  • Ruptured blood vessel leading to reduced blood flow
  • Intracerebral, subarachnoid, intraventricular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the risk factors of a stroke?

A
  • Hypertension
  • Age: the average age for a stroke is 68 to 75 years old
  • Smoking
  • Diabetes
  • Hypercholesterolaemia
  • Atrial fibrillation
  • Vasculitis
  • Family history
  • Haematological disease: such as polycythaemia
  • Medication: such as hormone replacement therapy or the combined oral contraceptive pill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical manifestations of a stroke affecting the anterior cerebral artery?

A

Contralateral hemiparesis and sensory loss with lower limbs > upper limbs

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

What are the clinical manifestations of a stroke affecting the middle cerebral artery?

A
  • Contralateral hemiparesisandsensorylosswith upper limbs > lower limbs
  • Homonymous hemianopia
  • Aphasia: if affecting the ‘dominant’ hemisphere (the left in 95% of right-handed people)
  • Hemineglect syndrome: if affecting the ‘non-dominant’ hemisphere; patients fail to be aware of items to one side of space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the clinical manifestations of a stroke affecting the posterior cerebral artery?

A
  • Contralateral homonymous hemianopiawithmacular sparing
  • Contralateralloss of pain and temperature due to spinothalamic damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the clinical manifestations of a stroke affecting the vertebrobasilar artery?

A
  • Cerebellarsigns
  • Reduced consciousness
  • Quadriplegiaorhemiplegia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the clinical manifestations of a stroke due to Weber’s syndrome (midbrain infarct)?

A

Oculomotor palsy and contralateral hemiplegia

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

What are the clinical manifestations of a stroke due to lateral medullary syndrome (posterior inferior cerebellar artery occlusion)?

A
  • Ipsilateralfacial loss of pain and temperature
  • IpsilateralHorner’s syndrome: miosis (constriction of the pupil), ptosis (drooping of the upper eyelid), and anhidrosis (absence of sweating of the face)
  • Ipsilateralcerebellar signs
  • Contralateralloss of pain and temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the Bamford classification?

A

The Bamford classification is commonly used and categorises stroke based on the area of circulation affected.

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

What blood vessels are involved in, and what is the criteria for, a total anterior circulation stroke (TACS)?

A
  • Anterior or middle cerebral artery.
  • All three of:
    • Hemiplegia
    • Homonymous hemianopia
    • Higher cortical dysfunction, such as dysphagia or neglect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What blood vessels are involved in, and what is the criteria for, a partial anterior circulation stroke (PACS)?

A
  • Anterior or middle cerebral artery.
  • Two of the three from the following:
    • Hemiplegia
    • Homonymous hemianopia
    • Higher cortical dysfunction, such as dysphagia or neglect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What blood vessels are involved in, and what is the criteria for, a lacunar stroke?

A
  • Perforating arteries: usually affects the posterior limb of the internal capsule.
  • There is no higher cortical dysfunction or visual field abnormality.
  • One of the following
    • Pure hemimotor or hemisensory loss
    • Pure sensorimotor loss
    • Ataxic hemiparesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What blood vessels are involved in, and what is the criteria for, a posterior circulation stroke?

A
  • Posterior cerebral or vertebrobasilar artery, or branches.
  • One of the following:
    • Cerebella syndrome
    • Isolated homonymous hemianopia
    • Loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the ROSIER scale and what is the criteria?

A
  • Recognition of Stroke in the Emergency Room
  • Loss of consciousness (-1)
  • Seizure activity (-1)
  • Asymmetric facial weakness (+1)
  • Asymmetric arm weakness (+1)
  • Asymmetric leg weakness (+1)
  • Speech disturbance (+1)
  • Visual disturbance field (+1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the investigations for a stroke?

A
  • Non-contrast CT of the head - FIRST LINE / GOLD STANDARD
  • CT angiogram
  • MRI of the head - alternative to CT
  • Bloods
    • FBC
    • Serum glucose
    • U&Es
    • Cardiac enzymes
    • PTT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the differential diagnoses for stroke?

A
  • Hypoglycaemia
  • Hyponatraemia
  • Hypercalcaemia
  • Uraemia
  • Hepatic encephalopathy
  • Brain tumours
  • Seizures
  • Complicated migraine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the management for a suspected ischemic stroke?

A
  • Stabilisation and referral - FIRST LINE
  • Give supplemental oxygen
  • Send to stroke unit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the management for confirmed ischemic stroke?

A
  • IV Alteplase for thrombolysis
  • Thrombectomy depending on the NIH stroke score
  • Anticoagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the management for prevention confirmed ischemic stroke?

A
  • Clopidogrel 75mg daily - FIRST LINE
  • Aspirin or subsequently dipyridamole alone as combination is contraindicated.
  • High dose statin - Atorvastatin
  • Manage hypertension, diabetes, smoking, other cardiovascular risk factors
  • Lifestyle advice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the complications of stroke?

A
  • DVT
  • Aspiration pneumonia
  • Neurological sequalae
  • Depression
  • Fatigue
  • Seizures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the management for a suspected haemorrhagic stroke?

A
  • Stabilisation and referral - FIRST LINE
  • Give supplemental oxygen
  • Send to stroke unit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the management for a confirmed haemorrhagic stroke?

A
  • Immediate referral for neurosurgery management
    • Craniotomy
    • Stereotactic aspiration
  • Stop anticoagulant or antithrombotic medication immediately
    • Warfarin
    • Dabigatran
    • Factor Xa inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Wernicke-Korsakoff syndrome?

A
  • Wernicke’s encephalopathy is a neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations.
  • Wernicke–Korsakoff syndrome is the combined presence of Wernicke encephalopathy and alcoholic Korsakoff syndrome.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the risk factors of Wernicke-Korsakoff syndrome?

A
  • Alcohol abuse
  • Malnutrition
  • Anorexia
  • Malabsorption due to stomach cancer and IBD
  • Prolonged vomiting e.g. due to chemotherapy, hyperemesis gravidarum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the clinical manifestations of Wernicke’s encephalopathy?

A
  • Ophthalmoplegia: weakness or paralysis of the eye muscles, nystagmus; lateral rectus; conjugate gate palsies
  • Ataxia or unsteady gait
  • Changes in mental state e.g. confusion, apathy, and difficulty concentrating
  • May also present with hypotension, hypothermia and reduced consciousness.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the clinical manifestations of Wernicke-Korsakoff syndrome?

A
  • Mainly targets the limbic system, causing severe memory impairment:
    • Anterograde amnesia: inability to create new memories
    • Retrograde amnesia: inability to recall previous memories.
    • Confabulation: creating stories to fill in the gaps in their memory which they believe to be true.
    • Behavioural changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the investigations for Wernicke-Korsakoff syndrome?

A
  • Diagnosis is typically based upon clinical presentation
  • Bloods
    • LFTs
    • Thiamine levels
    • Blood alcohol level
  • Red cell transketolase test - low
  • MRI/CT can confirm diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the differential diagnoses for Wernicke-Korsakoff syndrome?

A
  • Alcohol intoxication
  • Alcohol withdrawal
  • Encephalitis
  • Miller-Fisher syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is anterograde amnesia?

A

The inability to make new memories.

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

What is retrograde amnesia?

A

The inability to recall previous memories.

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

What is the management for Wernicke-Korsakoff syndrome?

A
  • IV thiamine alongside glucose
  • Followed by oral supplementation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the complications of Wernicke-Korsakoff syndrome?

A
  • Untreated Wernicke’s encephalopathy can lead to:
    • Hearing loss
    • Seizures
    • Spastic paraparesis
    • Coma
    • Death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is a migraine?

A

Migraine is a chronic, genetically determined, episodic neurological disorder that usually presents in early-to-mid life.

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

What are the risk factors for a migraine?

A
  • Family history
  • Female gender: migraines are three times more common in women
  • Obesity
  • Other important triggersinclude tiredness, lack of food, dehydration, menstruation, red wine and bright lights
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the triggers of migraines?

A
  • CHOCOLATE
  • CHocolate
  • Oral Contraceptives
  • alcOhoL
  • Anxiety
  • Travel
  • Exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the clinical manifestations of migraine?

A
  • Headache - severe unilateral pulsating, throbbing pain aggravated by movement
  • Nausea and Vomiting
  • Photophobia - sensitivity to light
  • Phonophobia - sensitivity to sounds
  • With or without aura
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is aura in relation to a headache?

A
  • Aura - term used to describe visual changes associated with migraines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is typical aura and what are the associated manifestations?

A
  • Typical aura: develops over 5 minutes, lasts 5-60 minutes and is fully reversible
    • Visual symptoms e.g. distortion, lines, dots, zigzag lines, scotoma
    • Paresthesia
    • Speech disturbance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is atypical aura and what are the associated manifestations?

A
  • Atypical aura: may last more than 60 minutes
    • Motor weakness (e.g. hemiplegic migraine - dysarthria, ataxia, ophthalmoplegia,
      hemiparesis)
    • Diplopia
    • Visual symptoms affectingoneeye
    • Poor balance (e.g. vestibular migraine)
    • Decreased level of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the investigations for a migraine?

A
  • Migraine is a clinical diagnosis
  • Fulfils the International Classification of Headache Disorders (ICHD)-3
  • Investigations are to rule out another pathology:
    • CT or MRI of the head
    • ESR
    • Lumbar puncture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the differential diagnoses for a migraine?

A
  • Stroke
  • Other primary headaches
  • Secondary headaches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is the management for an acute migraine?

A
  • Analgesia - ibuprofen or aspirin or paracetamol - FIRST LINE
  • Oral triptan alone (e.g. oral sumatriptan)+/- paracetamol or an NSAID
  • Antiemetics e.g. metoclopramide or prochlorperazine
  • AVOID OPIATES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the management for severe migraines?

A
  • FIRST LINE - Triptan e.g. Sumatripan
  • SECOND LINE - Ergot alkaloid
  • THIRD LINE - Corticosteroid
  • FOURTH LINE - Butalbital-containing compounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is the prophylactic management for chronic migraines?

A
  • Headache diary
  • FIRST LINE - propranolol (beta blocker)
  • Topiramate (anti-epileptic) - contraindicated in pregnancy
  • Amitriptyline (tri-cyclin antidepressant)
  • Frovatriptan or Zolmitriptan
  • Mindfulness, acupuncture, riboflavin (vitamin B2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What are the complications of migraines?

A
  • Depression
  • Migraine-triggered seizures
  • Migrainous infarction
  • Status migrainosus: a severe, debilitating migraine lasting for more than 72 hours that may warrant admission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the POUND mnemonic for migraines?

A
  • Criteria for the diagnosis of migraine.
  • P - Pulsatile headache
  • O - One-day duration
  • U - Unilateral
  • N - Nausea
  • D - Disabling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is a tension headache?

A

Tension-type headaches is a common primary headache disorder and can be either episodic or chronic.

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

What are the risk factors for a tension headache?

A
  • Stress
  • Bad posture
  • Sleep deprivation
  • Eye strain
  • Depression
  • Alcohol
  • Skipping meals
  • Dehydration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the clinical manifestations of a tension headache?

A
  • Bilateral with a pressing/tight sensation of mild-moderate intensity
    • Frequency varies depending on type of headache: chronic or episodic
  • Other associated symptoms:
    • Nausea or vomiting
    • Photophobia
    • Phonophobia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the investigations for a tension headache?

A
  • It is a clinical diagnosis based on criteria outlined by the International Headache Society
  • Other investigations to rule out other pathology
    • CT or MRI of the head
    • ESR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the differential diagnoses of a tension headache?

A
  • Other primary headaches
  • Secondary headaches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the management for an episodic/acute tension headache?

A
  • Analgesia e.g. paracetamol or NSAIDs - FIRST LINE
  • Limit the use of analgesia to no more than 6 days a month to reduce
    chance of medication-overuse headache
  • Lifestyle - evaluation of stress, depression, anxiety and sleep disorder.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the management for chronic tension headaches?

A
  • Antidepressants e.g. Amitriptyline - FIRST LINE
  • Muscle relaxants e.g. Tizanidine - SECOND LINE
  • Lifestyle - evaluation of stress, depression, anxiety and sleep disorder.
  • If no improvement then refer to neurology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What is a cluster headache?

A
  • Cluster headaches are intensely painful, unilateral, periorbital headaches with associated autonomic dysfunction.
  • Headaches occur in clusters:
    • Clusters usually last2 weeks to 3 months, separated byremissionperiods lasting at least3 month
    • Patients experience1 to 8 attacks per day
    • Clusters typically occur1 to 2 times per year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the risk factors for a cluster headache?

A
  • Male: 3 times more common in males
  • Family history - Autosomal dominant gene has a role
  • Smoking
  • Alcohol excess
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the investigations for a cluster headache?

A
  • Diagnosis is predominantly based on clinical presentation
    • At least 5 headache attacks fulfilling the symptomatic criteria
  • Investigations to rule out other pathology:
    • CT or MRI of the brain
    • ESR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the symptoms of a cluster headache?

A
  • Unilateral, periorbital or temporal headaches lasting 15 minutes to 3 hours
  • Ipsilateralautonomicsymptoms:
    • Lacrimation (teary eye)
    • Conjunctival injection (red eye due to enlargement of conjunctival vessels)
    • Nasal congestion
    • Rhinorrhoea (nasal discharge)
    • Ptosis (eyelid drooping)
    • Miosis (excessive constriction of the pupil of the eye)
    • Facial sweating
  • Nausea and vomiting
  • Photophobia, with agitation and restlessness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the differential diagnoses for a cluster headache?

A
  • Other primary headaches
  • Secondary headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the management for an acute cluster headache?

A
  • Triptans e.g. SubQ Sumatriptan (75% response rate within 15 minutes)
  • High-flow O2 (70% response rate within 15 minutes)
  • Drugs that should be avoided - paracetamol, NSAIDs, Opioids, Ergots, Oral Triptans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the prophylactic management for a cluster headache?

A
  • Verapamil - FIRST LINE
  • Lithium
  • Prednisolone - short course for two or three weeks to break the cycle during clusters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the complications of cluster headaches?

A
  • Mental illness: depression, anxiety, self-harm and suicide
  • Auto-enucleation: individuals attempting to remove the affected eye due to a belief that the pain will subside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is trigeminal neuralgia?

A

Trigeminal neuralgia is a pain syndrome which describes severe unilateral pain in the distribution of one or more trigeminal branches.

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

What are the risk factors for trigeminal neuralgia?

A
  • Advancing age: rare in people younger than 40 years of age
  • Female gender:more common in women
  • Demyelinating disease: trigeminal neuralgia is 20 times more common in patients with multiple sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the clinical manifestations of trigeminal neuralgia?

A
  • Facial pain: comes on spontaneously and last anywhere between a few seconds to hours.
  • Lacrimation
  • Facial swelling
  • Rhinorrhoea
  • Ptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the red flag features of trigeminal neuralgia?

A
  • May suggest a serious underlying cause:
    • Age of onsetbefore 40 years
    • Pain only in theophthalmic division(eye socket, forehead, and nose), orbilaterally
    • Sensorychanges
    • Deafnessor other ear problems
    • History ofskin or oral lesionsthat could spread perineurally
    • Optic neuritis
    • Family history of multiple sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the investigations of trigeminal neuralgia?

A
  • Trigeminal neuralgia is a clinical diagnosis
  • Investigations to rule out other pathology
    • MRI of the brain
    • Intra-oral X-ray (if pain from a dental origin is suspected)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the management for trigeminal neuralgia?

A
  • Anti-convulsant e.g. Carbamazepine - FIRST LINE
  • Baclofen - SECOND LINE
  • Refer to neurology
  • Microvascular decompression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is a medication overuse headache?

A

Overuse of medication causing headaches.

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

What are the clinical manifestations of a medication overuse headache?

A
  • Similar to that of a tension headache.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the diagnostic criteria for a medication overuse headache?

A
  • Headache occurring on 15 or more days per month in a person with a pre-existing headache disorderAND
  • Regular overuse for more than 3 months of one or more drugs that can be taken for acute and/or symptomatic treatment of headache.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the management for a medication overuse headache?

A
  • Withdrawal of analgesia
  • Discussion with or referral to a neurologist if overuse of opiates or tranquilisers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is Alzheimer’s disease?

A

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that causes significant deterioration in mental performance.

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

What are the risk factors for Alzheimer’s disease?

A
  • Age - old age is a major risk
  • Genetics / Family history
  • Cardiovascular disease: smoking and diabetes increase risk.Exercise decreasesrisk.
  • Depression
  • Low educational attainment
  • Low social engagement and support
  • Others: head trauma, learning difficulties
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the cognitive manifestations of Alzheimer’s disease?

A
  • Poor memory
  • Language problems: receptive and expressive dysphasia
  • Problems with executive functioning: planning and problem solving
  • Disorientation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the cognitive manifestations of Vascular dementia?

A
  • Poor memory
  • Language problems: receptive and expressive dysphasia
  • Problems with executive functioning: planning and problem solving
  • Disorientation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the behavioural and psychological manifestations of Alzheimer’s disease?

A
  • Agitation and emotional lability
  • Depression and anxiety
  • Sleep cycle disturbance
  • Disinhibition: social or sexually inappropriate behaviour
  • Withdrawal/apathy
  • Motor disturbance: wandering is a typical feature of dementia
  • Psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are the behavioural and psychological manifestations of vascular dementia?

A
  • Agitation and emotional lability
  • Depression and anxiety
  • Sleep cycle disturbance
  • Disinhibition: social or sexually inappropriate behaviour
  • Withdrawal/apathy
  • Motor disturbance: wandering is a typical feature of dementia
  • Psychosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the daily living problems of Alzheimer’s disease?

A
  • Loss of independence: increasing reliance on others for assistance with personal and domestic activities
  • Early stages: problems with higher level function (e.g. managing finances, difficulties at work)
  • Later stages: problems with basic personal care (e.g. washing, eating, toileting) and motor function (e.g. walking, transferring)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the daily living problems of vascular dementia?

A
  • Loss of independence: increasing reliance on others for assistance with personal and domestic activities
  • Early stages: problems with higher level function (e.g. managing finances, difficulties at work)
  • Later stages: problems with basic personal care (e.g. washing, eating, toileting) and motor function (e.g. walking, transferring)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the investigations for Alzheimer’s disease?

A
  • Cognitive assessment: e.g. mini mental state examination (MMSE)/ Montreal cognitive assessment scale (MoCA)
  • FBC
  • Metabolic panel
  • Vitamin B12
  • Urine drug screen
  • MRI or CT - will show medial temporal lobe atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the differential diagnoses for Alzheimer’s disease?

A
  • Other dementias
  • Depression
  • Delirium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is the management for Alzheimer’s disease?

A
  • Supportive therapy - FIRST LINE
  • Mild-to-moderate AD: acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine).
  • Moderate-to-severe AD: N-methyl-D-aspartic acid receptor antagonist (e.g. memantine). May be used in combination with acetylcholinesterase inhibitors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is vascular dementia?

A

Vascular dementia is a chronic progressive disease of the brain bringing about cognitive impairment. It is a common form of dementia caused by cerebrovascular disease.

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

What are the causes of vascular dementia?

A
  • Ischemic stroke
  • Small vessel disease
  • Haemorrhage
  • Leukaraiosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are the specific clinical manifestations of vascular disease?

A
  • Symptoms of dementia appear suddenly and brain function decline is step-wise (e.g. decreases with each stroke)
  • Symptoms of vascular dementia vary depending on which region of the brain is damaged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the investigations of vascular disease?

A
  • Clinical diagnosis based upon comprehensive history and physical examination
  • Neuropsychological tests: e.g. mini mental state exam, used to confirm loss of brain function
  • FBC
  • ESR
  • Blood glucose
  • LFTs
  • B12
  • TFTs
  • Medication review
  • CT or MRI of the brain - shows multiple cortical and subcortical infarcts and changes e.g. atrophy of the brain cortex, confirming ischaemia
  • ECG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is the management for vascular disease?

A
  • Supportive therapy - FIRST LINE
  • Antiplatelet therapy - FIRST LINE
  • Acetylcholinesterase inhibitors e.g. donepezil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What is frontotemporal dementia?

A
  • Frontotemporal dementia is a neurodegenerative disorder characterised by focal degeneration of the frontal & temporal lobes.
  • FTD is a heterogeneous condition with various subtypes e.g. Pick’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the risk factors for frontotemporal dementia?

A
  • Family history
    • MAPT gene (chromosome 17)
    • GRN gene (chromosome 17)
    • C9ORF72 gene (chromosome 9)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What are the frontal lobe effects of frontotemporal dementia?

A
  • Frontal lobe effects: personality and behaviour changes
    • Disinhibition(e.g. socially inappropriate behaviour)
    • Loss of empathy
    • Apathy(losing interest and/or motivation)
    • Hyperorality(e.g. dietary changes, attempt to consume non-edible products, eat beyond satiety)
    • Compulsive behaviour(e.g. cleaning, checking, hoarding)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What are the temporal lobe effects of frontotemporal dementia?

A
  • Temporal lobe effects: language problems
    • Effortful speech
    • Halting speech
    • Speech-sound errors
    • Speech apraxia(i.e. difficulty in articulation)
    • Word-finding difficulty
    • Surface dyslexia or dysgraphia: mispronouncing difficult words (e.g. yacht)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the investigations for frontotemporal dementia?

A
  • MRI - GOLD STANDARD - frontal and temporal love atrophy
  • Diagnosis is based upon cognitive assessment
  • Brain biopsy - NOT RECOMENDED - only way to obtain definitive diagnosis, typically done after death (presence of Pick’s bodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the management for frontotemporal dementia?

A
  • Supportive therapy - FIRST LINE
  • SSRI’s - may help with behavioural symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What is Lewy Body dementia?

A
  • Lewy body dementia is a neurodegenerative disease.
  • It is a type of dementia characterised by fluctuating cognitive impairment, visual hallucinations and parkinsonism.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What are the risk factors for Lewy Body dementia?

A
  • Older age
  • Male sex
  • Family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What are the early symptoms of Lewy Body dementia?

A
  • Early symptoms are typically cognitive ones (Alzheimer’s-like)
    • Difficulty focusing
    • Poor memory
    • Visual hallucinations
    • Disorganized speech
    • Depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the late symptoms of Lewy Body dementia?

A
  • Later symptoms are typically motor ones (Parkinson’s-like)
    • Resting tremors
    • Stiff and slow movements
    • Reduced facial expressions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the investigations for Lewy Body dementia?

A
  • Diagnosis of Lewy body dementia is based on the pattern of symptoms
  • Single-photon emission computer tomography (SPECT)
  • MRI or CT
  • Exclude other cause of symptoms:
    • FBC
    • U&Es
    • MSU
    • ESR
    • Serum B12
    • Folate
    • Glucose
    • Thiamine
    • Ca2+
    • TSH
  • Diagnosis can only be confirmed with a brain autopsy - shows Lewy Bodies in neurons.
  • Lewy bodies look like dark, eosinophilic inclusions in brainstem and neocortex.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the differential diagnoses for Lewy Body dementia?

A
  • Alzheimer’s
  • Parkinson’s
  • Frontotemporal dementia
  • Vascular dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is the management for Lewy Body dementia?

A
  • Supportive care - FIRST LINE
  • Dopamine analogue e.g. Levodopa
  • Cholinesterase inhibitors e.g. Donepezil
  • Avoid using antipsychotics as there is increased risk of side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is Parkinson’s disease?

A

Parkinson’s Disease (PD) is a neurodegenerative disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta (SNPC) of the basal ganglia (nigrostriatal pathway).

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

What are the risk factors for Parkinson’s disease?

A
  • Age:prevalence of 1% in those aged 60-70 and up to 1-3% in those ≥80 years old
  • Gender:males are 1.5 times more likely than females to develop PD
  • Family History
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are the motor symptoms of Parkinson’s disease?

A
  • Bradykinesia
  • Tremor
  • Rigidity
  • Micrographia
  • Hypomimia
  • Postural instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the non-motor symptoms of Parkinson’s disease?

A
  • Anosmia (smell blindness)
  • Sleep disturbance: REM sleep is impaired
  • Psychiatric symptoms
    • Depression
    • Anxiety
    • Dementia: usually develops after motor symptoms, unlike in Lewy-body dementia
  • Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What are the investigations for Parkinson’s disease?

A
  • PD is a clinical diagnosis: it should be suspected in a patient who has bradykinesiaand atleastoneofthe following:
    • Tremor
    • Rigidity
    • Postural instability
  • MRI of the brain - exclude other diseases
  • SPECT
  • Dopaminergic agent trial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What are the differential diagnoses for Parkinson’s disease?

A
  • Essential benign tremor
  • Metabolic abnormalities
  • Lewy Body dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the management for Parkinson’s disease?

A
  • Motor symptoms are affecting quality of life - Levodopa + decarboxylase inhibitor
    • Co-benyldopa (levodopaandbenserazide)
    • Co-careldopa (levodopaandcarbidopa)
  • Motor symptoms are NOT affecting quality of life - Dopamine agonist (Pramipexole, ropinirole), Monoamine oxidase B inhibitor (Selegiline, rasagiline), Levodopa + decarboxylase inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the complications of Parkinson’s disease?

A
  • Motor fluctuations
  • Dyskinesia - Dystonia, Chorea, Athetosis
  • Psychiatric complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is Parkinsonism?

A
  • Parkinsonism consists of a constellation of symptoms including:
    • Bradykinesia
    • Tremor
    • Rigidity
    • Postural instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is Huntington disease?

A

Huntington’s chorea is an autosomal dominant genetic neurodegenerative condition that causes a progressive deterioration in the nervous system.

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

What are the clinical manifestations of Huntington disease?

A
  • Patients are usually asymptomatic until symptoms begin around aged 30 to 50. It presents with an insidious, progressive worsening of symptoms.
    • Typically begins with prodromal phase: cognitive, psychiatric or mood problems.
    • Chorea(involuntary, abnormal movements)
    • Eye movement disorders
    • Dysarthria: speech difficulties
    • Dysphagia: swallowing difficulties
    • Dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the investigations of Huntington disease?

A
  • Diagnosis is made in a specialist genetic centre using a genetic test for the faulty gene and identification of the number of CAG repeats.
    • This involves pre-test and post-test counselling regarding the implications of the results.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the management for Huntington disease?

A
  • Counselling - FIRST LINE
  • Speech and language therapy
  • Medical treatment is for symptomatic relief:
    • For disordered movements
      • Antipsychotics (e.g. olanzapine)
      • Benzodiazepines (e.g. diazepam)
      • Dopamine-depleting agents (e.g. tetrabenazine)
    • For depression
      • Antidepressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the triple repeat disorders?

A
  • Huntington disease: CAG repeat
  • Myotonic dystrophy: CTG repeat
  • Friedreich ataxia: GAA repeat
  • Fragile X syndrome: CGG repeat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is MS?

A

Multiple sclerosis (MS) is an autoimmune, cell-mediated demyelinating disease of the central nervous system.

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

What are the risk factors for MS?

A
  • Age: most commonly diagnosed in 20-40 year olds
  • Female gender: MS is 3 times more common in females
  • Smoking
  • Obesity
  • Vitamin D deficiency
  • Northern latitudes
  • Family history: HLA-DR2 is implicated; 30% monozygotic twin concordance
  • Autoimmunity: patients often have a family history of other autoimmune disorders
  • EBV infection: the virus with the greatest link to MS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

What are the signs of MS?

A
  • Optic neuritis
  • Double vision
  • Internuclear ophthalmoplegia and conjugate lateral gaze disorder
  • Upper motor neuron signs with spastic paraparesis are common
  • Cerebellar signs: such as ataxia and tremor
  • Sensory loss: due to demyelination of spinothalamic or dorsal columns
  • Trigeminal neuralgia: stimulation to face causes pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are the signs of MS?

A
  • Optic neuritis
  • Double vision
  • Internuclear ophthalmoplegia and conjugate lateral gaze disorder
  • Upper motor neuron signs with spastic paraparesis are common
  • Cerebellar signs: such as ataxia and tremor
  • Sensory loss: due to demyelination of spinothalamic or dorsal columns
  • Trigeminal neuralgia: stimulation to face causes pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are the symptoms of MS?

A
  • Blurred vision and red desaturation
  • Numbness, tingling and other strange sensations: plaques in the sensory pathways
  • Weakness
  • Bowel and bladder dysfunction: plaques involve the autonomic nervous system
  • Lhermitte’s phenomenon: electric shock sensation on neck flexion, caused by stretching the demyelinated dorsal column.
  • Uhtoff’s phenomenon: worsening of symptoms following a rise in temperature, such as a hot bath
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are the investigations for MS?

A
  • MRI brain and spine - GOLD STANDARD - Shows multiple CNS lesions
  • Lumbar puncture - oligoclonal bands in CSF and increased IgG
  • Visual evoked potentials
  • FBC - normal
  • Metabolic panel - normal
  • TSH - normal
  • Vitamin B12 - normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is the McDonald criteria?

A
  • The McDonald criteria is used to diagnose MS.
  • In brief, the criteria can be described assymptoms/signs which demonstrate dissemination in space (i.e. different parts of the CNS affected) and time.
  • The main diagnostic criteria:
    • Diagnosis is based on:
      • 2 or more relapsesAND EITHER
        • Objective clinical evidence of 2 or more lesionsOR
        • Objective clinical evidence of one lesionWITHa reasonable history of a previous relapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the general management for MS?

A
  • MDT care
  • Legally need to inform the DVLA
  • Supportive therapy - lifestyle changes, regular exercise and good sleep hygiene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the relapse management for MS?

A
  • Corticosteroids - Oral or IV methylprednisolone - FIRST LINE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is the chronic management for MS?

A
  • Beta-interferon
  • Alemtuzumab (anti-CD52) and natalizumab (anti-alpha4beta1-integrin)
  • Glatiramer acetate
  • Fingolimod
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are the complications of MS?

A
  • Genitourinary:urinary tract infections, urinary retention and incontinence
  • Constipation
  • Depression: offer mental health support if required
  • Visual impairment
  • Mobility impairment: offer physiotherapy, orthotics and other mobility aids
  • Erectile dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is Guillain-Barre syndrome?

A
  • Guillain-Barré syndrome is an acute paralytic polyneuropathy.
  • It is an autoimmune, rapidly progressive demyelinating condition of the peripheral nervous system, often triggered by infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What are the risk factors for Guillain-Barre syndrome?

A
  • Male:slightly more common in males than females (1.8:1)
  • Age:peak incidence between 15-35 years old and 50-75 years old
  • Infections:typically gastrointestinal or respiratory:
    • Bacterial:e.g. Campylobacter jejuni (30%) and mycoplasma pneumoniae
    • Viral:e.g. Zika virus, influenza, Epstein-Barr virus and cytomegalovirus
  • Malignancies:lymphoma may increase the risk of GBS
  • Vaccines:association with the influenza vaccination (uncommon)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What are the signs of Guillain-Barre syndrome?

A
  • Reduced sensation in affected limbs
  • Symmetrical weakness in lower extremities first, progressing to the upper limbs
  • Ataxia with hypoflexia (or areflexia) in affected limbs
  • Autonomic dysfunction
  • Respiratory distress
  • Cranial nerve involvement and bulbar dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What are the symptoms of Guillain-Barre syndrome?

A
  • Tingling and numbness in hands and feet: often precedes muscle weakness
  • Symmetrical, progressive, ascending weakness
  • Unsteady when walking
  • Back and leg pain: common at some point in disease course
  • Shortness of breath
  • Facial weakness and speech problems
141
Q

What are the investigations for Guillain-Barre syndrome?

A
  • Predominantly a clinical diagnosis evidenced by progressive weakness and areflexia (or hyporeflexia) in the weaker limbs. The Brighton criteria is used for diagnosis.
  • Bloods to exclude other causes
    • FBC
    • U&Es
    • TFTs
    • LFTs
    • Anti-ganglioside antibodies
  • Spirometry
  • Cultures
  • Lumbar punctures
  • Nerve conduction studies
142
Q

What are the differential diagnoses of Guillain-Barre syndrome?

A
  • Transverse myelitis
  • Myasthenia gravis
  • Lambert-eaton myasthenic syndrome
  • Botulism
  • Polymyositis
  • Vasculitic neuropathy
143
Q

What is the management for Guillain-Barre syndrome?

A
  • IV immunoglobulins (IVIg) - FIRST LINE
  • Plasma exchange - FIRST LINE
  • Thromboprophylaxis
  • Physiotherapy
  • Intensive care support:for those who develop ventilatory failure (20%), intensive care and mechanical ventilation may be required
144
Q

What are the complications of Guillain–Barre syndrome?

A
  • Type 2 respiratory failure
  • Impaired mobility
  • Pulmonary complications
  • Autonomic dysfunction
  • Psychiatric impact
145
Q

What is Charcot-Marie-Tooth disease?

A

Charcot-Marie-Tooth disease is a group of inherited diseases that affects the peripheral motor and sensory nerves.

146
Q

What are the signs of Charcot-Marie-Tooth disease?

A
  • Pes cavus: high foot arches
  • Hammer toes: the middle joint of a toe bends upwards
  • Distal muscle wasting causing inverted champagne bottle legs
  • Hand and arm muscle wasting causing claw hand
  • Thickened palpable nerves e.g. common peroneal
147
Q

What are the symptoms of Charcot-Marie-Tooth disease?

A
  • Symptoms usually start to appear before the age of 10 years but the onset of symptoms can be delayed until 40 or later.
  • Weakness in the lower legs, particularly loss ofankle dorsiflexion
    • Foot drop
    • High-stepped gait
  • Weakness in the hands
  • Reduced tendon reflexes
  • Reduced muscle tone
  • Peripheral sensory loss
  • Tingling and burning sensations in the hands and feet
  • May be neuropathic pain
148
Q

What are the investigations of Charcot-Marie-Tooth disease?

A
  • Genetic testing - GOLD STANDARD
  • Nerve conduction studies - FIRST LINE
  • Bloods - FBC, LFTs, TFTs, B12 and Folate
  • Hip X-ray - normal or hip dysplasia
149
Q

What are the differential diagnoses for Charcot-Marie-Tooth disease?

A
  • Diabetic neuropathy
  • Chronic inflammatory demyelinating polyneuropathy
  • Acquired peripheral neuropathy
  • Hereditary spastic paraplegia
  • Spino-cerebellar degeneration
150
Q

What is the management for Charcot-Marie-Tooth syndrome?

A
  • Physiotherapists - FIRST LINE
  • Occupational therapist
  • Podiatrist
  • Orthopaedic surgery - correct disabling joint deformities
151
Q

What are primary brain tumours?

A
  • A brain tumour is an abnormal growth occurring in any tissue contained within the cranium, including the brain, cranial nerves, meninges, skull, pituitary gland, and pineal gland.
  • There are many different types of brain tumours. They vary from benign tumours (e.g. meningiomas) to highly malignant (e.g. glioblastomas).
152
Q

What are primary brain tumours?

A
  • A brain tumour is an abnormal growth occurring in any tissue contained within the cranium, including the brain, cranial nerves, meninges, skull, pituitary gland, and pineal gland.
  • There are many different types of brain tumours. They vary from benign tumours (e.g. meningiomas) to highly malignant (e.g. glioblastomas).
153
Q

How are primary brain tumours graded?

A

The scale goes from I to IV based on the morphologic and functional features of the tumour cells; a grade IV tumour being the most abnormal looking cells that also tend to be the most aggressive.

154
Q

What are the 5 types of primary brain tumour?

A
  • Gliomas
    • Astrocytoma
    • Oligodendroglioma
    • Ependymoma
  • Meningiomas
  • Pituitary adenoma
  • Hemangioblastomas
  • Acoustic neuroma (AKA vestibular Schwannoma)
155
Q

What are the clinical manifestations of raised intercranial pressure?

A
  • Headache: worse on waking, coughing and bending
  • Vomiting
  • Altered mental state
  • Visual field defects
  • Seizures (particularly focal)
  • Unilateral ptosis
  • Third and sixth nerve palsies
  • Papilloedema (on fundoscopy)
156
Q

What are the clinical manifestations of primary brain tumours?

A
  • Headaches
  • Nausea
  • Vomiting
  • Seizures
  • Focal neurological symptoms - depends on location of tumour
  • Signs of ICP
157
Q

What are the investigations for primary brain tumours?

A
  • CT/ MRI - FIRST LINE
  • Blood tests e.g. FBC, U&Es, LFT’s, B12
  • Tissue biopsy: to determine cancer grade and guide management - GOLD STANDARD
158
Q

What are the differential diagnoses for primary brain tumours?

A
  • Other causes of space-occupying lesion:
    • Aneurysm
    • Abscess
    • Cyst
    • Haemorrhage
    • Idiopathic intracranial hypertension
159
Q

What is the management for primary brain tumours?

A
  • Steroids e.g. IV Dexamethasone: to reduce oedema/ inflammation
  • Surgery (dependent on the grade and behaviour of the brain tumour)
  • Chemotherapy
  • Radiotherapy
  • Palliative care
160
Q

What are the complications of primary brain tumours?

A
  • Hydrocephalus: as the tumour grows it can compress nearby cells and structures e.g. as meningiomas enlarge they can compress the ventricles and block CSF flow causing hydrocephalus
  • Midline shift and herniations through foramen magnum: due to rising pressures
161
Q

What are the common secondary brain tumours?

A
  • Lung - Small lung and non-small small cell
  • Breast
  • Melanoma
  • Renal cell
  • GI
162
Q

What are the investigations for secondary brain tumours?

A
  • CT or MRI - GOLD STANDARD
163
Q

What is the management for secondary brain tumours?

A
  • Steroids e.g. dexamethasone: reduce cerebral oedema
  • Stereotactic radiotherapy/ chemotherapy
  • Surgery if <75 years
  • Palliative care
164
Q

What is Cauda Equina syndrome?

A
  • Cauda equina syndrome (CES) is a neurosurgical emergency which occurs when the bundle of nerves below the end of the spinal cord are compressed.
165
Q

What are the signs o Cauda Equine syndrome?

A
  • Bilateral lower limb weakness and/or reduced sensation
  • Decreased or absent lower limb reflexes
  • Reduced perianal sensation (S2-S4) and anal tone on examination
  • Palpable bladder due to urinary retention
166
Q

What are the symptoms of Cauda Equina syndrome?

A
  • Lower back pain and sciatica (97%)
  • ‘Saddle anaesthesia’: numbness in the peri-anal region, groin and inner thighs (93%)
  • Bladder and bowel dysfunction: urinary retention or incontinence (92%), or rarely faecal incontinence
  • Leg weakness and difficulty walking/ paralysis of the legs
    • Leg weakness if flaccid and hypo-reflexic/ areflexic (lower motor neuron signs)
  • Erectile dysfunction
167
Q

What are the investigations for Cauda Equina syndrome?

A
  • Examinations: PR exam, knee reflexes, ankle reflexes etc
  • Rectal exam - FIRST LINE
  • MRI spine - GOLD STANDARD
  • Bladder ultrasound
  • CT myelography - if contraindications of MRI
168
Q

What are the differential diagnoses of Cauda Equine syndrome?

A
  • Conus medullaris syndrome
  • Vertebral fracture
  • Peripheral neuropathy
  • Mechanical lower back pain
169
Q

What is the management for Cauda Equina syndrome?

A
  • EMERGENCY decompressive laminectomy
  • Antibiotics for abscess
  • Corticosteroids or radiotherapy
170
Q

What are the complications of Cauda Equina syndrome?

A
  • Complications of delayed presentation or decompression
  • DVT
  • Post-operative complications
171
Q

What is the difference in pathology between conus medullaris syndrome and cauda equina syndrome?

A
  • CMS - Damage to the spinal cord at vertebral level T12-L2
  • CES - Damage to the spinal cord at vertebral level L1-L5
172
Q

What is the difference in features between conus medullaris syndrome and cauda equina syndrome?

A
  • CMS - Often presents with upper motor neuron signs (e.g. hyperflexia and hypertonia)
  • CES - Usually presents with lower motor neuron signs (hyporeflexia and hypotonia)
173
Q

What is meningitis?

A
  • Meningitis describes inflammation of the leptomeninges (the arachnoid and pia mater) and usually occurs due to a bacterial, viral, or fungal infection.
  • Bacterial meningitis and meningococcal disease are notifiable diseases in England
174
Q

What pathogens are the most common cause of meningitis?

A

N. meningitidis and S. pneumoniae are the commonest causes of bacterial meningitis in the UK, whilst enteroviruses such as coxsackievirus are the most common cause of viral meningitis.

175
Q

What are the bacterial causes of meningitis?

A
  • Neonatal:group B streptococcus,E. coli,Listeria monocytogenes
  • Children:N. meningitidis,S. pneumoniae,H. influenzae
  • Adults:S. pneumoniae,N. meningitidis
  • Immunocompromised: Listeria monocytogenes, M. tuberculosis
176
Q

What are the viral causes of meningitis?

A
  • Enteroviruses: coxsackievirus and echovirus
  • Herpes simplex virus (HSV):HSV-2 meningitis is more common than HSV-1
  • Varicella-zoster virus (VZV)
177
Q

What are the fungal causes of meningitis?

A
  • Cryptococcus neoformans
  • Candida
178
Q

What are the risk factors for meningitis?

A
  • Immunocompromised patients
  • Non-immunised patients
  • Crowded environment
179
Q

What are the signs of meningitis?

A
  • Kernig’s sign: when the hip is flexed and the knee is at 90°, extension of the knee results in pain
  • Brudzinski sign: severe neck stiffness causes the hips and knees to flex when the neck is flexed
  • Petechial or purpuric non-blanching rash: associated with meningococcal disease (N. meningitidis)
  • Pyrexia
  • Reduced GCS
180
Q

What are the symptoms of meningitis?

A
  • Meningism
    • Headache
    • Photophobia
    • Neck stiffness
  • Fever
  • Nausea and vomiting
  • Seizures
  • Symptoms can develop quickly or over several days, but typically occur within 3 to 7 days of exposure to the pathogen.
181
Q

What are the investigations for meningitis?

A
  • Lumbar puncture - GOLD STANDARD
    • CSF gram stain
    • CSG culture
    • CSF PCR
  • FBC
  • CRP
  • Coagulation screen
  • Blood glucose
  • Blood culture
  • Whole-blood PCR
182
Q

What is the management for bacterial meningitis?

A
  • Antibiotics - depends on local guidelines
    • Cephalosporins - IV Cefotaxime or IV Ceftriaxone
    • > 50 or immunocompromised add IV Amoxicillin (to cover listeria)
  • Steroids - dexamethasone
183
Q

What is the management for viral meningitis?

A
  • Supportive treatment
  • Self-liming in 4-40 days
  • Acyclovir in HSV or VZV caused meningitis
184
Q

What is the management for fungal meningitis?

A

Cryptococcal meningitis - IV Amphoteracin B

185
Q

What is the prophylactic management for meningitis?

A
  • Ciprofloxacin: asingle500mg dose of oral ciprofloxacin - FIRST LINE
  • Rifampicin:SECOND LINE as it requires > 1 dose and interferes with other medications
186
Q

What are the complications of meningitis?

A
  • Abscess
  • Cerebral oedema
  • Hydrocephalus and brain herniation
  • Seizures
  • Sensorineural hearing loss
  • Memory loss
  • Cerebral palsy
  • Long-term cognitive and behaviour deficit
  • Waterhouse-Freidrichsen syndrome
  • Sepsis
187
Q

What is encephalitis?

A

Encephalitis describes inflammation of the brain parenchyma. It mostly affects frontal and temporal lobes.

188
Q

What are the risk factors for encephalitis?

A
  • Immunocompromised
  • Blood/fluid exposure:HIV and West Nile virus
  • Mosquito bite: West Nile virus
  • Transfusion and transplantation: CMV, EBV, HIV
  • Close contact with cats: toxoplasmosis
189
Q

What are the signs of encephalitis?

A
  • Pyrexia
  • Reduced GCS
  • Focal neurological deficit, such as:
    • Aphasia
    • Hemiparesis
    • Cerebellar signs
  • May also have signs of meningitis: meningio-encephalitis
190
Q

What are the symptoms of encephalitis?

A
  • Fever
  • Headache
  • Fatigue
  • Confusion
  • Seizures
  • Behavioural changes:
    • Memory disturbance
    • Psychotic behaviour
    • Withdrawal or change in personality
191
Q

What are the investigations for encephalitis?

A
  • Bloods
    • FBC
    • CRP
    • U&Es
    • Blood culture
  • Contrast CT or MRI
  • Lumbar puncture and CSF investigations
  • HIV serology
  • EEG
192
Q

What are the differential diagnoses for encephalitis?

A
  • Meningitis
  • Encephalopathy
  • Status epilepticus
  • CNS vasculitis
193
Q

What is the management for encephalitis?

A
  • Antiviral medication:
    • Acyclovir - FIRST LINE
    • Ganciclovir and Foscarnet if CMV infection
  • Further management will depend on the underlying organism
194
Q

What are the complications of encephalitis?

A
  • Seizures
  • Ischaemic stroke
  • Hydrocephalus: accumulation of cerebrospinal fluid (CSF) within the brain
  • Lasting fatigue and prolonged recovery
  • Aphasia
  • Change in personality or mood
  • Changes to memory and cognition
  • Learning disability
  • Headaches
  • Chronic pain
  • Movement disorders
  • Sensory disturbance
  • Hormonal imbalance
195
Q

What is Herpes Zoster?

A

Herpes zoster (HZ) (shingles) is caused by reactivation of varicella-zoster virus (VZV) that was acquired during a primary varicella infection, and is characterised by dermatomal pain and papular rash.

196
Q

What are the clinical manifestations of Herpes Zoster?

A
  • Macular-vesicular rash in dermatomal distribution
    • Usually in a single stripe of vesicles around either the left or the right side of the body or on one side of the face.
    • Crust formation and drying occurs over the next week with resolution in 2-3 weeks
  • Pain, itching, or tingling in the area where the rash is
  • Malaise, myalgia, headache and fever can be present
  • Disseminated infection may occur, if immunosuppressed
197
Q

What are the investigations of Herpes Zoster?

A
  • Shingles are usually diagnosed based on clinical presentation of the skin lesions
  • Diagnosis confirmed with: viral PCR, culture, immunohistochemistry
    • Tzanck test: look for multinucleated giant cells in the fluid of the vesicles
    • Look for varicella zoster antibodies or viral DNA.
198
Q

What is the management for Herpes Zoster?

A
  • Oral aciclovir/ valaciclovir
  • IV aciclovir if pregnant, immunosuppressed or severe/ disseminated infection
  • Topical antibiotic treatment for secondary bacterial infection
  • Oral/ topical analgesics
199
Q

What is motor neurone disease?

A

Motor neurone disease is an umbrella term that encompasses a variety of specific diagnoses. It is a cluster of degenerative disease characterised by axonal degeneration of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells.

200
Q

What are the types of motor neurone disease?

A
  • Amyotrophic lateral sclerosis: UMN + LMN
  • Progressive muscular atrophy: LMN only
  • Primary lateral sclerosis: UMN only
  • Progressive bulbar palsy: LMN only
201
Q

What are the risk factors for motor neurone disease?

A
  • Advancing age
  • Male gender: 1.2 to 1.8 times more likely to develop MND
  • Family history: familial in 5% of cases and the SOD1 mutation is implicated
  • Smoking: currently a ‘probable’ risk factor for MND
  • Exposure to heavy metals and certain pesticides
202
Q

What are the signs of motor neurone disease?

A
  • Mixed UMN and LMN signs
  • Spastic paraparesis with brisk reflexes
  • Upgoing plantar responses
  • Fasciculations (twitches in the muscles) especially on the tongue
  • Dysarthria and dysphagia: particularly in progressive bulbar palsy
  • Muscle wasting: particularly of small hand muscles and tibialis anterior
  • Reduced tone
203
Q

What are the symptoms of motor neurone disease?

A
  • Progressive weakness often first noticed in the upper limbs
  • Clumsiness
  • Fatigue
  • Falls
  • Speech and swallow issues: particularly in progressive bulbar palsy
204
Q

What are the investigations for motor neurone disease?

A
  • El Escorial criteria - GOLD STANDARD
  • MND is a clinical diagnosis
  • Investigations to rule out other pathology
    • Electromyography
    • Nerve conduction studies
    • MRI of the spine
    • Lumbar puncture
    • Pulmonary function tests
205
Q

What are the differetnial diagnoses for motor neurone disease?

A
  • Multiple sclerosis
  • Polyneuropathies
  • Myasthenia gravis
  • Diabetic amyotrophy
  • Guillain-Barre syndrome
  • Spinal cord tumours
206
Q

What is the management for motor neurone disease?

A
  • Riluzole and supportive care - FIRST LINE
  • Respiratory support - BiPAP
  • Supportive treatment:
    • Antispasmodics: such as baclofen
    • Analgesia
    • Feeding support: many patients require nutritional support, often with PEG tube
    • Speech and language therapy
    • Physiotherapy
    • Advanced directivesto document the patients wishes as the disease progresses
    • End of life careplanning
207
Q

What is myasthenia gravis?

A

Myasthenia gravis is a chronic autoimmune disorder of the postsynaptic membrane at the neuromuscular junction of skeletal muscle.

208
Q

What are the risk factors for myasthenia gravis?

A
  • Female gender: twice as common in women
  • Familyhistory
  • Autoimmunity: either a personal or family history of autoimmune disorders such as rheumatoid arthritis and SLE
  • Thymoma or thymic hyperplasia: 10-15% of patients have a thymoma, whilst up to 70% have thymic hyperplasia
209
Q

What are the signs of myasthenia gravis?

A
  • Proximal muscle weakness with fatigability: often affecting the face and neck
  • Ptosis (drooping eyelid)
  • Complex ophthalmoplegia
  • Head drop - rare sign
  • Myasthenic snarl - snarling expression when attempting to smile
210
Q

What are the symptoms of myasthenia gravis?

A
  • Lethargy
  • Muscle weakness: worsens throughout the day, can improve with rest
  • Diplopia: double vision due to effects on eye muscles
  • Slurred speech
  • Dysphagia: difficulty swallowing
  • Fatigue in jaw when chewing
  • Shortness of breath: may suggest a myasthenic crisis
211
Q

What are the investigations for myasthenia gravis?

A
  • Based upon a clinical diagnosis - FIRST LINE
  • Antibodies:AchR antibodies are GOLD STANDARD
  • anti-MuSK and anti-LRP4 - GOLD STANDARD if AchR is negative
  • CT or MRI at the thymus - for thymoma
  • Thyroid function
  • Serial pulmonary function tests
  • Tensilon test
  • Crushed ice test
212
Q

What are the differential diagnoses for myasthenia gravis?

A
  • Lambert-Eaton myasthenic syndrome
  • Botulism
  • Penicillamine-induced myasthenia gravis
  • Primary myopathies
213
Q

What is the management for stable patients with myasthenia gravis?

A
  • Acetylcholinesterase inhibitor e.g. Pyridostigmine - FIRST LINE
  • Prednisolone - SECOND LINE
  • Azathioprine - THIRD LINE
  • Other - methotrexate or rituximab
  • Thyroidectomy
214
Q

What is the management of a myasthenic crisis?

A
  • IV immunoglobulin or plasmapheresis
  • Intubation:if severe respiratory compromise
  • Corticosteroidsmay be used as an adjunct
215
Q

What are the complications of a myasthenic crisis?

A
  • Myasthenic crisis: weakening of the respiratory muscles and is often provoked by infections or medications. Patients present with increasing shortness of breath, which can deteriorate into respiratory failure.
  • Respiratory failure
  • Aspiration pneumonia: dysphagia increases the risk of aspiration
216
Q

What is Lambert-Eaton myasthenic syndrome?

A
  • Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of the neuromuscular junction in the peripheral nervous system.
  • It may occur as a paraneoplastic disorder in association with cancer, usually a small cell carcinoma of the lung, or may occur without cancer, as part of a more general autoimmune state.
217
Q

What are the risk factors for Lambert-Eaton myasthenic syndrome?

A
  • Can be associated with other autoimmune diseases e.g. Hashimoto’s thyroiditis or diabetes mellitus type 1.
  • Small cell lung cancer malignancy
  • Smoking
  • Family history of autoimmune disease
218
Q

What are the clinical manifestations of Lambert-Eaton myasthenic syndrome?

A
  • Symmetrical proximal muscle weakness, especially proximal leg muscle weakness
  • Diplopia: double vision due to effect on intraocular muscles
  • Ptosis: drooping of eyelids due to effect on levator muscles
  • Slurred speech: due to effect on oropharyngeal muscles
  • Dysphagia: due to effect on oropharyngeal muscles
  • Reduced tendon reflexes
219
Q

What are the investigations for Lambert-Eaton myasthenic syndrome?

A
  • Test for autoantibodies against voltage-gated calcium channels
  • Electromyography
  • Chest X-ray / CT scan - for small cell lung cancer
  • Nerve conduction studies
220
Q

What are the differential diagnoses for Lambert-Eaton myasthenic syndrome?

A
  • Botulism
  • Myasthenia gravis
  • Myopathy
  • Chronic inflammatory demyelinating neuropathy
  • Guillain-Barre syndrome
221
Q

What is the management for Lambert-Eaton Myasthenic syndrome?

A
  • Manage underlying malignancy
  • Pyridostigmine/ amifampridine
  • Immunosuppressants
  • IV immunoglobulins
  • Plasmapheresis
222
Q

What are the complications of Lambert-Eaton myasthenic syndrome?

A
  • Respiratory failure: when respiratory muscles are affected
  • Aspiration: due to impaired swallowing
  • Amifampridine related seizures
  • Osteoporosis: related to corticosteroid use
223
Q

What is carpal tunnel syndrome?

A

Carpal tunnel syndrome (CTS) is a collection of symptoms and signs caused by compression of the median nerve in the carpal tunnel.

224
Q

What are the risk factors for carpal tunnel syndrome?

A
  • Female > Male: due to same size tendon but in smaller wrist.
  • Age: Usually in those over 30 years old.
225
Q

What are the clinical manifestations of carpal tunnel syndrome?

A
  • Pain: worse at night after a day’s use of hands
  • Numbness
  • Paraesthesia: relieved by hanging hand over bed and shaking it (wake and shake)
  • Muscle weakness in the hands
  • Tinels, Phalens and Durkans sign: +ve
  • Light touch, 2-point discrimination and sweating can be impaired
226
Q

What is Phalen’s manoeuvre?

A

Flex the wrists are far as possible and hold that position for a minute, this results in numbness in the areas of the hand innervated by the median nerve in people with carpal tunnel syndrome

227
Q

What is Tinel’s sign?

A

Tap the transverse carpal ligament, this reproduces the symptoms of tingling or feelings of pins and needles in areas of the hand served by the median nerve

228
Q

What is Durkan’s sign?

A

Manually compressing the carpal tunnel with the thumb for 30 second, to reproduce symptoms of carpal tunnel

229
Q

What are the investigations for carpal tunnel syndrome?

A
  • Tinels, Phalens and Durkans sign: +ve - clinical diagnosis
  • Electromyography - GOLD STANDARD
  • Ultrasound or MRI of the wrist
230
Q

What is the management for carpal tunnel syndrome?

A
  • Behavioural modification e.g. changing positioning of hand when typing etc
  • Physical therapy
  • Mild-Moderate/Pregnant
    • Wrist splint - FIRST LINE
    • Corticosteroid injection - SECOND LINE
  • Severe
    • Surgical decompression - FIRST LINE
231
Q

What is Sciatica?

A
  • Sciatica is where the sciatic nerve, which runs from your lower back to your feet, is irritated or compressed.
    • Leading to pain from the lower back down to the lower leg.
  • Pain is associated with injury or compression of the sciatic nerve.
232
Q

What are the clinical manifestations of sciatica?

A
  • Aching and sharp leg pain which radiates to the middle or lower buttock and outer thigh.
  • Unilateral (Bilateral is a red flag for cauda equina syndrome)
  • Numbness
  • Motor weakness
  • Loss of reflexes
  • Loss of ankle jerk reflex - S1 spinal nerve compression.
  • Loss of knee jerk reflex - L4 nerve compression.
233
Q

What are the investigation for sciatica?

A
  • Lasegu’s sign positive
  • CT or MRI of the spine - GOLD STANDARD
234
Q

What is Lasegu’s sign?

A
  • Examiner raises straight leg which stretches nerve root over the herniated disk.
  • If pain worsens when leg is between 30-70 degrees then the diagnosis is conformed.
235
Q

What is the differential diagnosis for sciatica? and what are the complications?

A
  • Cauda Equina
  • Paralysis
236
Q

What is the management for sciatica?

A
  • Sciatic pain usually resolves on it’s own over time but the pain can be relieved with pain medication
  • Analgesia (NOT opioids)
  • NASIDs
  • If symptoms worsen
    • Amitriptyline
    • Duloxetine
  • Specialist management
    • Epidural corticosteroid injections.
    • Local anaesthetic injections.
    • Radiofrequency denervation.
    • Spinal decompression.
    • Surgical treatment for tumours, cysts or injury to spinal cord.
237
Q

What is foot drop?

A

Foot drop is a result of weakness of the foot dorsiflexors.

238
Q

What are the causes of foot drop?

A
  • Common peroneal nerve lesion is the most common cause.
  • L5 radiculopathy.
  • Sciatic nerve lesion.
  • Superficial or deep peroneal nerve lesion.
  • Other possible includes central nerve lesions (e.g. stroke) but other features are
    usually present.
239
Q

What are the risk factors of foot drop?

A
  • Leg crossing
  • Kneeling
240
Q

What are the signs of foot drop?

A
  • If the patient has isolated peroneal neuropathy there will be weakness of foot dorsiflexion and eversion → Reflexes will be normal.
  • Weakness of hip abduction is suggestive of a L5 radiculopathy.
241
Q

What are the symptoms of foot drop?

A
  • Steppage gait - drag their toes while walking
  • Unilateral symptoms
  • Tripping over
  • Numbness and weakness in the same side
  • In some cases skin on top of foot and toes feels numb
242
Q

What are the investigations of foot drop?

A
  • Clinical diagnosis - FIRST LINE
  • Imaging - X-ray, CT or MRI
  • Nerve conduction study
243
Q

What is the management for foot drop?

A
  • Brace and Splint.
  • Physiotherapy.
  • Specialised shoes → prevents foot drop when walking.
  • Nerve stimulation.
  • Surgery if indicated.
244
Q

What is wrist drop?

A
  • Wrist dropis a medical condition in which thewristand thefingers cannot extend at themetacarpophalangeal joints
  • The characteristic deformity of a radial nerve lesion
245
Q

What are the causes of wrist drop?

A
  • Radial nerve injury - stab wounds to the chest.
  • Compression of the radial nerve.
  • Brachial plexus injury.
  • Fracture or dislocation of the humerus.
  • Neurological conditions such as multiple sclerosis, polio, or amyotrophic lateral sclerosis (ALS).
246
Q

What is the management for wrist drop?

A
  • Wrist splint
  • Surgical removal of bone or anatomical defects (if from compression)
247
Q

What are the differential diagnoses for wrist drop?

A
  • C7 root injury
  • Posterior interosseous neuropathy
248
Q

What would weakness of the brachioradialis, wrist extension and finger flexion indicate?

A
  • A radial nerve lesion
249
Q

What would weakness of finger extension and radial deviation of the wrist on extension?

A
  • Posterior interosseous nerve lesion
250
Q

What would weakness of triceps, finger extension and flexors indicate?

A
  • C7 and C8 lesion
251
Q

What would general weakness of the upper limb marked in deltoid, triceps, wrist extension and finger extension?

A
  • Corticospinal lesion.
252
Q

What is management for wrist drop?

A
  • Wrist splint
  • Surgical removal of bone or anatomical defects (if from compression)
253
Q

What is a differential diagnoses for wrist drop?

A
  • C7 root injury
  • Posterior interosseous neuropathy
254
Q

What is claw hand?

A
  • Deformity where the fingers are bent into a position that looks like a claw.
  • Results in hyperextension at the metacarpophalangeal joints and flexion of the interphalangeal joints.
  • Also known as ulnar claw and spinster’s claw.
255
Q

What are the causes of claw hand?

A
  • Brachial plexus lesion (C8-T1).
  • Other spinal cord lesions eg syringomyelia, polio.
  • Volkmann’s contracture.
  • Rheumatoid arthritis (advanced, untreated disease).
  • Ulnar and median nerve lesion.
256
Q

What are the two types of claw hand?

A
  • Complete - results from bothUlnar and Median Nerve Palsy, involves all digits.
  • Partial (or incomplete) - involves only ulnar 2 digits and is referred to as anisolated Ulnar Nerve Palsy.
257
Q

What is the management for claw hand?

A

Surgery - Nerve repair or decompression if possible.

258
Q

What is spinal cord compression?

A
  • Spinal cord compression (SCC) results from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself.
  • This is a medical emergency as it can lead to paralysis.
259
Q

What are the clinical manifestations of spinal cord compression?

A
  • Back pain: radicular pain (spinal/ root pain) may precede weakness and sensory loss
  • Progressive weakness of legs (typically symmetrical) with UMN signs e.g. contralateral spasticity and hyperreflexia
  • Sensory loss 1-2 cord segments below level of lesion
  • UMN signs below the level of lesion
  • LMN signs at level of lesion
  • Signs dependent on level of lesion e.g.
    • L5/S1 lesion = sciatica (sensory loss and pain in back of thigh/ leg/ lateral aspect of little toe)
    • L4/L5 lesion = L5 nerve root compression (sensory loss/pain in lateral thigh/lateral leg & medial side of big toe)
  • Bladder and anal sphincter involvement: a late sign; hesitancy, frequency and painless retention
260
Q

What are the investigations of spinal cord compression?

A
  • MRI of spine - GOLD STANDARD
  • Biopsy/surgical exploration
  • Screening blood tests: FBC, ESR, B12, U&Es, LFT, PSA
  • Chest X-ray - Check for TB
261
Q

What are the differential diagnoses for spinal cord compression?

A
  • Transverse myelitis
  • Multiple sclerosis
  • Carcinomatous meningitis
  • Cord vasculitis
  • Spinal artery thrombosis/ aneurysm
  • Trauma
  • Guillain-Barre syndrome
262
Q

What is the management for spinal cord compression?

A
  • Steroids e.g. IV dexamethasone
  • Laminectomy or microdiscectomy
  • Chemotherapy if indicated
  • Analgesia
263
Q

What is amaurosis fugax?

A
  • A classical syndrome of painless short-lived monocular blindness.
  • It is a term usually reserved for transient visual loss of ischaemic origin.
264
Q

What are the causes of amaurosis fugax?

A
  • Occurs due to the temporary reduction in the retinal, ophthalmic or ciliary blood flow leading to temporary retinal hypoxia.
  • The principle cause of amaurosis fugax is transient obstruction e.g. due to emboli, of the ophthalmic artery, which is a branch of the internal carotid artery.
  • However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion.
265
Q

What is syncope?

A
  • Syncope is the term used to describe the event of temporarily losing consciousness due to a disruption of blood flow to the brain, often leading to a fall.
  • Syncopal episodes are also known as vasovagal episodes, or simply fainting.
266
Q

What are the risk factors of syncope?

A
  • Elderly
  • Pregnant women
  • Certain medications that
    • Block vasoconstriction e.g. calcium channel blockers, beta blockers, alpha blockers, and nitrates
    • Affect the volume status e.g. diuretics
    • That prolong the QT interval e.g. antipsychotics and antiemetics
  • Anxiety and panic disorders
  • Alcohol abuse
  • Drug abuse
267
Q

What is neuropathy?

A
  • A pathological process affecting a peripheral nerve or nerves
268
Q

What is mononeuropathy?

A
  • A process affecting a single nerve
269
Q

What is mononeuritis multiplex?

A
  • Usually describes a condition that affects several nerves, but in no discernible pattern, and no underlying unifying condition. i.e. the nerves have been individually damaged.
270
Q

What is polyneuropathy?

A
  • Many nerves involved. Usually describes a symmetrical disease, and it usually begins distally. Can be sensory, motor or mixed. Classified into demyelinating, or axonal types. Loads of different types and different classifications. Often widespread loss of tendon reflexes is typical, with distal weakness and distal sensory loss
271
Q

What are the sympathetic presentations of peripheral neuropathy?

A
  • Postural hypotension
  • Reduced sweating
  • Ejaculatory failure
  • Horner’s syndrome
272
Q

What are the parasympathetic presentations of peripheral neuropathy?

A
  • Erectile dysfunction
  • Constipation
  • Nocturnal diarrhoea
  • Urine retention
  • Holmes-Adie pupil
273
Q

What are the specific causes of peripheral neuropathy?

A

The mnemonicDAVIDcan be used:

  • D – Diabetes
  • A – Alcoholism
  • V – Vitamin Deficiency – B12
  • I – Infective / inherited – Guillian-Barre / Charcot-Marie-Tooth
  • D – Drugs – e.g. isoniazid
274
Q

What is depression?

A
  • A disorder that causes persistent feelings of low mood, low energy and reduced interest.
  • Persistent depressive disorder is characterised by at least 2 years of a depressed mood for most of the day, for more days than not, for at least 2 years.
275
Q

What are the risk factors for depression?

A
  • Older age
  • Recent child birth (postpartum depression)
  • Trauma
  • Co-existing conditions
  • Family history of depression
  • Medications e.g. corticosteroids
  • Female sex
276
Q

What are the signs and symptoms of depression?

A
  • Low/Depressed mood
  • Anhedonia - a lack of pleasure in activities
  • Low energy
  • Anxiety and worry
  • Irritability
  • Avoiding social situations (e.g. school)
  • Hopelessness about the future
  • Poor sleep, particularly early morning waking
  • Poor appetite or over eating
  • Poor concentration
  • Reduced libido
  • Weight changes
277
Q

What are the investigations for depression?

A
  • Clinical diagnosis - ICD-11 or DSM-5-TR diagnostic criteria depending on the subcategory
  • Bloods - FBC, Metabolic panel, TFTs, Patient health questionnaire
278
Q

What is the management for depression?

A
  • Antidepressant if mild or severe - First Line
    • e.g. Citalopram, Fluoxetine
    • Consider if mild
  • Psychotherapy or other non-pharmacological treatment
  • Immediate symptom management with benzodiazepines +/- antipsychotic
    • Emergency cases
  • Supportive treatments
279
Q

What is von Hippel-Lindau disease?

A

Von Hippel Lindau disease is a rare autosomal dominant disorder characterized by a mutation in a tumour suppressor gene which leads to the formation of cysts and benign tumours in various parts of the body like the eye, CNS, kidneys, adrenal glands and pancreas.

280
Q

What are the signs of a cranial nerve lesion?

A
  • The olfactory nerve
  • Reduced smell and taste
281
Q

What are the causes of a cranial nerve I lesion?

A
  • The olfactory nerve
  • Trauma
  • Frontal lobe tumour
  • Meningitis
282
Q

What are the signs of a cranial nerve II lesion?

A
  • The optic nerve
  • Visual field defects
  • Pupillary abnormalities
  • Optic neuritis
  • Optic atrophy
283
Q

What are the signs of a cranial nerve III lesion?

A
  • The oculomotor nerve
  • Fixed dilated pupils which don’t accommodate
  • Ptosis
  • Complete internal ophthalmoplegia
  • Unopposed lateral rectus causes outward deviation of the eye
284
Q

What are the causes of a cranial nerve III lesion?

A
  • The oculomotor nerve
  • Diabetes mellitus
  • Giant cell arteritis
  • Syphilis
  • Posterior communicating artery aneurysm
  • Idiopathic
  • Raised ICP (if uncal herniation through the tentorium - this compresses the nerve)
285
Q

What are the signs of a cranial nerve IV lesion?

A
  • The trochlear nerve
  • Diplopia due to weakness of downward and inward eye movement (pure vertical diplopia)
  • Compensation by tilting the head away from the affected side
286
Q

What are the causes of a cranial nerve IV lesion?

A
  • The trochlear nerve
  • Trauma to the orbit
  • Diabetes
  • Infarction secondary to hypertension
287
Q

What are the signs of a cranial nerve V lesion?

A
  • The trigeminal nerve
  • Reduced sensation or dysasthesia over the affected area
  • Weakness of jaw clenching and side-to-side movement.
  • If LMN lesion, the jaw deviates to the weak side when the mouth is opened
  • May be fasciculation of temporalis and masseter
288
Q

What are the causes of a cranial nerve V lesion?

A
  • The trigeminal nerve
  • Sensory:
    • Trigeminal neuralgia
    • Herpes zoster
    • Nasopharyngeal carcinoma
  • Motor:
    • Bulbar palsy
    • Acoustic neuroma
289
Q

What are the signs of a cranial nerve VI lesion?

A
  • The abducent nerve
  • Inability to look laterally
  • Eye is deviated medially because of unopposed action of the medial rectus muscle
290
Q

What are the causes of a cranial nerve VI lesion?

A
  • The abducent nerve
  • MS
  • Pontine CVA
291
Q

What are the signs of a cranial nerve VII lesion?

A
  • Facial nerve
  • Facial weakness
  • LMN lesion:
    • Forehead is paralysed - the final common pathway to the muscles is destroyed
  • UMN lesion:
    • Upper facial muscles are partially spared because of alternative pathways in the brainstem
292
Q

What are the signs of a cranial nerve VIII lesion?

A
  • Vestibulocochlear nerve
  • Unilateral sensorineural deafness
  • Tinnitus
  • Slow-growing lesions seldom present with vestibular symptoms as compensation has time to occur
  • Vertigo
  • Nystagmus
293
Q

What are the signs of a cranial nerve IX lesion?

A
  • Glossopharyngeal nerve
  • Unilateral lesions do not cause any deficit because of bilateral corticobulbar connections
  • Bilateral lesions result in pseudobulbar palsy
  • Loss of gag reflex
294
Q

What are the causes of a cranial nerve IX lesion?

A
  • Glossopharyngeal nerve
  • Trauma
  • Brainstem lesions
  • Cerebellopontine angle and neck tumours
  • Polio
  • Guillain-Barre syndrome (GBS)
295
Q

What are the signs of a cranial nerve X lesion?

A
  • Vagus nerve
  • Palatal weakness:
    • Nasal speech
    • Nasal regurgitation of food
    • Palate moves asymmetrically when the patient says ‘ahh’
  • Recurrent nerve palsy:
    • Hoarseness
    • Loss of volume
    • Bovine cough
296
Q

What are the causes of a cranial nerve X lesion?

A
  • Vagus nerve
  • Trauma
  • Brainstem lesions
  • Tumours in the cerebellopontine angle, jugular foramen and neck
  • Polio
  • GBS
297
Q

What are the signs of a cranial nerve XI lesion?

A
  • Accessory nerve
  • Weakness and wasting of the muscles which turn the head to the contralateral side
298
Q

What are the causes of a cranial nerve XI lesion?

A
  • Accessory nerve
  • Trauma
  • Brainstem lesions
  • Tumours in the cerebellopontine angle, jugular foramen and neck
  • Polio
  • GBS
299
Q

What are the signs of a cranial nerve XII lesion?

A
  • Hypoglossal nerve
  • LMN lesion:
    • Wasting of the ipsilateral side of the tongue, with fasciculation
    • Attempted protrusion of tongue causes deviation towards the affected side
300
Q

What are the causes of a cranial nerve XII lesion?

A
  • Polio
  • Syringomyelia tuberculosis
  • Median branch thrombosis of the vertebral artery
301
Q

What is epilepsy?

A

Epilepsy is an umbrella term for a condition where there is a tendency to have seizures. Seizures are transient episodes of abnormal electrical activity in the brain.

302
Q

What are the risk factors for epilepsy?

A
  • Cerebrovascular disease
  • Head trauma
  • Cerebral infections
  • Family history: epilepsy orneurological illness
  • Premature birth
  • Congenital malformations of the brain
  • Genetics conditions associated with epilepsy
303
Q

What is the diagnostic criteria for epilepsy?

A
  • Criteria 1:≥2 unprovoked (or reflex) seizures occurring more than 24 hours apart
  • Criteria 2: 1 unprovoked (or reflex) seizure with a probability of further seizures felt to be at a similar recurrence risk to patients with ≥2 unprovoked seizures over the next 10 years.
  • Criteria 3: A diagnosed epilepsy syndrome
304
Q

What are the investigations for epilepsy?

A
  • EEG - GOLD STANDARD
  • MRI or CT of the brain
  • ABG or VBG
  • ECG
  • Bloods
    • U&Es
    • Glucose
    • FBC
    • Blood cultures
    • Inflammatory markers
305
Q

What is the management for tonic-clonic seizures?

A
  • FIRST LINE - Sodium valproate
  • SECOND LINE - Lamotrigine or Carbamazepine
306
Q

What is the management for focal seizures?

A
  • FIRST LINE - CarbamazepineorLamotrigine
  • SECOND LINE - Sodium valproate or Levetiracetam
307
Q

What is the management for absence seizures?

A
  • FIRST LINE - Sodium valproate or Ethosuximide
308
Q

What is the management for atonic seizures?

A
  • FIRSR LINE - Sodium valproate
  • SECOND LINE - Lamotrigine
309
Q

What is the management for myoclonic seizures?

A
  • FIRST LINE - Sodium valproate
  • Other options
    • lamotrigine
    • Levetiracetam
    • Topiramate
310
Q

What is the management infantile spasms?

A
  • Prednisolone
  • Vigabatrin
311
Q

What is a further treatment option for seizures?

A
  • Epilepsy surgery: removal of cause of seizure e.g. specific part of the brain or tumour.
  • Nerve stimulation: certain nerves e.g. the vagus nerve are stimulated, which is thought to control seizures by influencing neurotransmitter release.
312
Q

What are the driving rules surrounding seizures?

A
  • Adults who present with anisolatedseizure:
    • Should stop driving for6 months, providingno cause is foundon brain imaging and there is no epileptiform activity on EEG
  • If the aboveconditions are not metor the patient has knownepilepsy:
    • Patients must be seizure-free for12 monthsbefore they may qualify for a driving license
    • If seizure-free for 5 years, a ‘til 70 licence is usually reinstated
  • Withdrawal of anti-epilepsy medication:
    • Patients must not drive if medication has been withdrawnandfor6 monthsafter the last dose
  • If the patientdrives a heavy goods vehicle (HGV):
    • They must be seizure-free for5 yearsbefore they can start driving
  • ALL PATIENTS MUST INFORM THE DVLA
313
Q

What are the two types of seizure?

A
  • When the affected area is limited to one hemisphere - or one half of the brain - or sometimes even a smaller area like a single lobe, it is known as a focal seizure.
  • A generalisedseizureis where both hemispheres of the brain are affected. These can be subcategorised.
314
Q

What is a tonic seizure?

A
  • Tonic seizure: the muscles become stiff and flexed, which can cause the patient to fall, usually backwards
315
Q

What is an atonic seizure?

A
  • Atonic seizures: aka drop attacks. The muscles suddenly relax and become floppy, which can cause the patient to fall, usually forward. These don’t usually last more than 3 minutes. They typically begin in childhood. They may be indicative ofLennox-Gastaut syndrome.
316
Q

What is a clonic seizure?

A
  • Clonic seizures: violent muscle contractions (convulsions).
317
Q

What is a tonic-clonic seizure?

A
  • Tonic-clonic seizures: there is loss of consciousness andtonic(muscle tensing) andclonic(muscle jerking) episodes. Typically the tonic phase comes before the clonic phase. There may be associated tongue biting, incontinence, groaning and irregular breathing.
318
Q

What is a myoclonic seizure?

A
  • Myoclonic seizures: short muscle twitches. The patient usually remains awake during the episode. They occur in various forms of epilepsy but typically happen in children as part ofjuvenile myoclonic epilepsy.
319
Q

What is an absence seizure?

A
  • Absence seizures: aka petit mal seizures, impaired awareness or responsiveness. Patient becomes blank and stares into space before returning to normal. Motor abnormalities are either absent or very minor e.g. eyelid flutters or repetitive lip smacking. Common in children. Most patients (> 90%) stop having absence seizures as they get older.
320
Q

What is status epilepticus?

A
  • Status epilepticus (SE) is a single, continuous seizure lasting more than five minutesortwo or more seizures within a five-minute periodwithoutregaining consciousness in between.
  • It is amedical emergency.
321
Q

What are four examples of non-epileptic seizures?

A
  • Psychogenic non-epileptic spells (PNES)
  • Convulsive syncope
  • Infantile spasms (West syndrome)
  • Febrile convulsions
322
Q

What is a subarachnoid haemorrhage?

A

Subarachnoid haemorrhage (SAH) is a type of intracranial haemorrhage characterised by blood within the subarachnoid space.

323
Q

What are the risk factors for a subarachnoid haemorrhage?

A
  • Increasing age: most commonly presents in people > 50 years old
  • Hypertension
  • Smoking
  • Alcohol excess: there is a significantly increased risk withcurrentalcohol abuse
  • Cocaine use
  • Family history
  • Polycystic kidney disease(PKD): 5 times more common in autosomal dominant PKD
  • Connective tissue disorders: such as Marfan syndrome or Ehlers-Danlos
  • Neurofibromatosis: tumours form on your nerve tissues
324
Q

What are the investigations for a subarachnoid haemorrhage?

A
  • Non-contrast CT - GOLD STANDARD
  • Lumbar puncture if CT is negative
  • CT angiogram
  • FBC
  • Serum glucose
  • Clotting screen
325
Q

What is the management for a subarachnoid haemorrhage?

A
  • CCB - Nimodipine - FIRST LINE
  • Surgery:
    • Endovascular coiling of the aneurysm
    • Surgical clipping via craniotomy
  • Shunt for hydrocephalus
326
Q

What are the complications of subarachnoid haemorrhage?

A
  • Re-bleeding (22 chance in the 1st month)
  • Vasospasm
  • Hydrocephalus
  • Seizures
  • Hyponatraemia
327
Q

What is a intracerebral haemorrhage? and what are the two types?

A
  • Intracerebral haemorrhage describes bleeding within the cerebrum.
  • Two types:
    • Intraparenchymal haemorrhage: involves just the brain tissue
    • Intraventricular haemorrhage: blood extends into the ventricles of the brain which store cerebrospinal fluid
328
Q

What are the risk factors of an intracerebral haemorrhage?

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
  • Anticoagulants such as warfarin
329
Q

What are the signs of a subarachnoid haemorrhage?

A
  • 3rd nerve palsy
    • An aneurysm arising from the posterior communicating artery will press on the 3rd nerve, causing apalsywith afixed dilated pupil
  • 6th nerve palsy
    • A non-specific sign which indicates raised intracranial pressure
  • Reduced GCS
330
Q

What are the symptoms of a subarachnoid haemorrhage?

A
  • Headache
    • Severe, sudden onset
    • Occipital
    • ‘Thunderclap’ headache
  • Meningism: photophobia and neck stiffness
  • Vision changes
  • Nausea and vomiting
  • Speech changes
  • Seizures
  • Weakness
  • Confusion
  • Coma
331
Q

What are the clinical manifestations of a intracerebral haemorrhage?

A
  • Headache
  • Weakness
  • Seizures
  • Vomiting
  • Reduced consciousness
  • Specific signs will depend on the area affected
332
Q

What are the investigation for a intracerebral haemorrhage?

A
  • Non-contrast CT of the head - GOLD STANDARD
  • Angiography
  • Check FBC and clotting factors
  • U&Es
333
Q

What is the management for intracerebral haemorrhage?

A
  • Consider intubation, ventilation and ICU care if they have reduced consciousness
  • Correct any clotting abnormality
  • Correct severe hypertension but avoid hypotension
  • Drugs to relieve intracranial pressure e.g. Mannitol
  • Craniotomy
  • Stereotactic aspiration
  • STOP ANTICOAGULANT OR ANTITHROMBOTIC MEDICATIONS
334
Q

What is a subdural haemorrhage?

A
  • Bleeding below the dura mater in the brain.
335
Q

What are the risk factors for subdural haemorrhage?

A
  • Head injury
  • Brain atrophy
  • Alcohol abuse
  • Hypertension
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
  • Anticoagulants such as warfarin
336
Q

What are the clinical manifestations of subdural haemorrhagge?

A
  • Reduced GCS: loss of consciousness right after the injury or in the ensuing days to weeks as the haematoma increases in size.
  • Headaches
  • Vomiting
  • Seizures
  • Sometimes there can be focal neurological symptoms e.g. muscle weakness, unequal pupils, hemiparesis or sensory problems
337
Q

What are the investigations for subdural haemorrhage?

A
  • Non-contrast CT - GOLD STANDARD
    • acute subdural haematoma
    • chronic subdural haematoma
    • midline shift
  • Check FBC and clotting
338
Q

What are the differential diagnoses for subdural haemorrhage?

A
  • Stroke
  • Dementia
  • CNS masses e.g. tumours or abscesses
  • Subarachnoid haemorrhage
  • Epidural haemorrhage
339
Q

What is the management for subdural haemorrhage?

A
  • Surgery - clot evacuation, craniotomy or burr holes
  • IV mannitol to reduce ICP
  • Reverse clotting abnormalities
340
Q

is an epidural (extradural ) haemorrhage?

A
  • Bleeding above the dura mater of the brain.
341
Q

What are the risk factors for an epidural (extradural) haemorrhage?

A
  • Head injury
  • Hypertension
  • Aneurysms
  • Ischaemic stroke can progress to haemorrhage
  • Brain tumours
  • Anticoagulants such as warfarin
342
Q

What are the clinical manifestations of a epidural (extradural) haemorrhage?

A
  • Reduced GCS: loss of consciousness right after the injury or in the ensuing days to weeks as the haematoma increases in size.
  • Headaches
  • Vomiting
  • Seizures
  • Sometimes there can be focal neurological symptoms e.g. muscle weakness, unequal pupils, hemiparesis or sensory problems
343
Q

What are the investigations for a epidural (extradural) haemorrhage?

A
  • CT or MRI scan
    • Hyperdense mass
    • -lemon mass’ shape - bi-convex
  • Check FBC and clotting
  • Skull X-ray - may show a fracture
344
Q

What are the differential diagnoses for a epidural (extradural) haemorrhage?

A
  • Epilepsy
  • Carotid dissection
  • Carbon monoxide poisoning
  • Subdural haematoma
  • Subarachnoid haemorrhage
345
Q

What is the management for a epidural (extradural) haemorrhage?

A
  • Urgent surgery - Craniotomy for clot evacuation and ligation of the vessel
  • IV mannitol to reduce ICP
  • Stabilise patient
346
Q

What is the glasgow coma scale?

A
  • TheGlasgow Coma Scale(GCS) is a universal assessment tool for assessing the level of consciousness.
  • It is scored based oneyes,verbalresponse andmotorresponse.
  • The maximum score is 15/15, minimum is 3/15. When someone has a score of 8/15 or below then you need to consider securing their airway as there is a risk they are not able to maintaining it on their own.
347
Q

What are the eye response scores for the GCS?

A
  • Spontaneous = 4
  • Speech = 3
  • Pain = 2
  • None = 1
348
Q

What are the verbal response scores for the GCS?

A
  • Orientated = 5
  • Confused conversation = 4
  • Inappropriate words = 3
  • Incomprehensible sounds = 2
  • None = 1
349
Q

What are the motor response scores for the GCS?

A
  • Obeys commands = 6
  • Localises pain = 5
  • Normal flexion = 4
  • Abnormal flexion = 3
  • Extends = 2
  • None = 1

Phase 2a Sheffield Medicine (10 decks)

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