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ΩΩ 3a Bateman - Neuro + Cardio > Neurology > Flashcards

Neurology Flashcards

1
Q

Why do you get a fixed pupil from a head injury?

A

Compression of the parasympathetic fibres on the optic nerve due to raisefd ICP

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2
Q

What does each spinal tract do?

A
  1. Dorsal column - Vibration and proprioception
  2. Spinaothalamic - pain, sensation and temp
  3. Corticospinal - Weakness
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3
Q

What is Brwon-sequard syndrome?

A
  1. Hemisection of the spinal cord - anterior white commisure
    • Ipsilateral paralysis
    • Ipsilateral loss of proprioception and fine discrimination
    • Contralateral loss of pain and temperature
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4
Q

ves How are headaches classified?

A
  1. Primary
  2. Secondary
  3. Cranial neuralgias
  4. Facial pain
  5. Other headaches
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5
Q

What are the primary headaches?

A

Tension

Migraine

Cluster

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6
Q

What are secondary headaches?

A

Headaches that arise from a cause, this includes:

Dental pain

Menengitis

Encephalitis

Traumatic head injury

Substance abuse

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7
Q

WHAT IS A MIGRAINE?

A

Severe throbbing pain or a pulsing sensation, usually on one side of the head

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8
Q

What causes migraines?

What are the triggers?

A

Exact cause unknown, but thought to be imbalances in brain chemicals

C - Chocolate
H - Hangovers
O - Orgasms
C - Cheese/Caffeine
O - Oral contraceptive pill
L - Lie-ins
A - Alcohol
T - Travel
E - Exercise

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9
Q

What are the stages of a migraine?

A
  • Prodrome
  • Aura
  • Attack
  • Post-drome
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10
Q

What are the symptoms of a migraine?

A

Migraine without aura
Most common
Headaches - one or both sides of the head
Sickness
Nausea
Photophobia
Phonophobia

Migraine with aura
Similar symptoms
Accompained by changes in vision, certain smells

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11
Q

How is a migraine diagnosed?

A

Usually a diagnosis based on medical history, symptoms and a neurological examination

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12
Q

What is the treatment for migraines?

A

Pain-relieving medications

  • Ibuprofen, paracetamol
  • Sumatriptan, rizatriptan

Preventive medications

  • Propanalol
  • Topiramate - Not in women who are child-bearing age
  • Verapamil - Blood pressure lowering meds
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13
Q

WHAT IS A TENSION HEADACHE?

A

A tension headache is generally a diffuse, mild to moderate pain in your head that’s often described as feeling like a tight band around your head.

Most common type of headache

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14
Q

What is the cause of tension headaches?

A

The cause of tension headaches is not known.

Experts used to think tension headaches stemmed from muscle contractions in the face, neck and scalp, perhaps as a result of heightened emotions, tension or stress.

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15
Q

What are the symptoms of a tension headache?

A

Dull, aching head pain

Sensation of tightness or pressure across your forehead or on the sides and back of your head

Tenderness on your scalp, neck and shoulder muscles

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16
Q

What are the different types of tension headache?

A

Episodic tension headaches

Episodic tension headaches can last from 30 minutes to a week. Frequent episodic tension headaches occur less than 15 days a month for at least three months. Frequent episodic tension headaches may become chronic.

Chronic tension headaches

This type of tension headache lasts hours and may be continuous. If your headaches occur 15 or more days a month for at least three months, they’re considered chronic.

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17
Q

How do you diagnose a tension headache?

A

Medical history

Physical and neurological examinations

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18
Q

What is the treatment for a tension headache?

A

Acute treatment

  • Aspirin, paracetamol or an NSAID are first-line

Prophylaxis

  • ‘Up to 10 sessions of acupuncture over 5-8 weeks’
  • Low-dose amitriptyline is widely used in the UK for prophylaxis against tension-type headache.
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19
Q

WHAT IS A CLSUTER HEADACHE?

A

Cluster headaches, which occur in cyclical patterns or cluster periods, are one of the most painful types of headache.

A cluster headache commonly awakens you in the middle of the night with intense pain in or around one eye on one side of your head.

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20
Q

What is the cause/triggers of a cluster headache?

A

Unknown

Possible triggers:
Alcohol

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21
Q

What are the symptoms of a cluster headache?

A
  1. Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
  2. Clusters typically last 4-12 weeks
  3. Intense sharp, stabbing pain around one eye (recurrent attacks ‘always’ affect same side)
  4. Accompanied by redness, lacrimation, lid swelling
  5. miosis and ptosis in a minority
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22
Q

How do you diagnose a cluster headache?

A

Clinical

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23
Q

What is the acute treatment for a cluster headache?

A

100% Oxygen

Subcutaenous triptan

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24
Q

What is the prophylaxtic treatment for a cluster headache?

A

Verapamil - Calcium channel blocker

Prednisolone

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25
Q

WHAT IS TEMPORAL ARTERITIS?

A

Giant cell arteritis is an inflammation of the lining of your arteries.

Most often, it affects the arteries in your head, especially those in your temples.

For this reason, giant cell arteritis is sometimes called temporal arteritis.

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26
Q

What is the pathophysiology of temporal arteritis?

What condition is it closely linked to?

A
  1. With giant cell arteritis, the lining of arteries becomes inflamed, causing them to swell.
  2. This swelling narrows your blood vessels, reducing the amount of blood — and, therefore, oxygen and vital nutrients — that reaches your body’s tissues
  3. Polymyalgia rheumatica
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27
Q

What are the symptoms of temporal arteritis?

A
  1. Persistent, severe head pain, usually in your temple area + jaw pain when you chew or open your mouth wide
  2. Scalp tenderness
  3. Fever
  4. Fatigue
  5. Unintended weight loss
  6. Vision loss or double vision, particularly in people who also have jaw pain
  7. Sudden, permanent loss of vision in one eye
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28
Q

What are the complications of temporal arteritis?

A
  1. Blindness
  2. Aortic aneurysm
  3. Stoke
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29
Q

How do you diagnose temporal artertitis?

A
  1. Blood tests
    • ESR
    • CRP
  2. Imaging
    • Doppler ultrasound
  3. Biopsy
    • Skip Lesions + Giant cells
  4. CK and EMG - Normal
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30
Q

What is the treatment for temporal arteritis?

A
  1. High dose corticosteroid
    • Prednisolone
  2. May prescribe vitamin D supplements to help prevent bone loss
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31
Q

WHAT IS A STROKE?

A

A stroke occurs when the blood supply to part of your brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients.

Brain cells begin to die in minutes.

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32
Q

What are the causes of a stroke?

A

Ischaemic stroke

Haemorrhagic stroke

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33
Q

What are the symptoms of a stroke?

A
  1. Motor weakness
  2. Speech problems (dysphasia)
  3. Swallowing problems
  4. Visual field defects (homonymous hemianopia)
  5. Balance problems
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34
Q

How do you diagnose a stroke?

A

Confirm diagnosis

  1. Non-contast CT is first line
  2. Hyperdense sign in an artery

Estalish the site of pathology

  1. Carotid ultrasound
  2. Echocardiogram
  3. Cerebral angiogram

Identify factors which may influence management

  1. Chest X-ray - cardiac enlargement
  2. Blood glucose - hyperglycaemia
  3. Full Blood Count - polycythaemia, thrombocytopenia
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35
Q

How do you investigate a carotid bruit?

A

Duplex ultrasound

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36
Q

What is the treatment for a stroke?

A

Ischaemic stroke

  1. Alteplase/tissue plasminogen factor within 4.5 hours
  2. Once haemorrhagic stroke has been excluded give aspirin 300mg
  3. Endovascular procedures - Thombectomy within 6 hours, an extended time of 6-24 hours may be considefed if CT shows salvagable tissue
  4. Thrombolysis and thrombectomy if under 4.5 hours

Haemorrhagic stroke

  1. Blood thinners
  2. Surgical clipping
  3. Coiling
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37
Q

What is the long term management following a stroke?

A
  1. Clopidogrel 75mg - FIRST LINE
  2. Aspirin + dipyridamole for patinet who cannot tolerate clopidogrel
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38
Q

What is a pontine haemorrhage?

A

Pontine haemorrhage is a life-threatening condition. It often occurs as a complication secondary to chronic hypertension

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39
Q

How do patients with a pontine haemorrhage usually present?

A
  1. Reduced Glasgow coma score
  2. Quadriplegia
  3. Miosis
  4. Absent horizontal eye movements
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40
Q

What is the cause of lateral medullary syndrome?

A

Posterior inferior cerebellar artery

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41
Q

WHAT IS A TRANSIENT ISCHAEMIC ATTACK (TIA)?

A

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

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42
Q

What is the cause of a TIA?

A

A transient ischemic attack has the same origins as that of an ischemic stroke, the most common type of stroke.

In an ischemic stroke, a clot blocks the blood supply to part of your brain.

In a transient ischemic attack, unlike a stroke, the blockage is brief, and there is no permanent damage.

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43
Q

What are the symptoms of a TIA?

A
  1. Weakness, numbness or paralysis in your face, arm or leg, typically on one side of your body
  2. Slurred or garbled speech or difficulty understanding others
  3. Blindness in one or both eyes or double vision
  4. Vertigo or loss of balance or coordination
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44
Q

How do you investigate a TIA?

A
  1. Brain Imaging
    • CT brain should not be done ‘unless there is clinical suspicion of an alternative diagnosis that CT could detect’
    • MRI is preferred to determine the territory of ischaemia, or to detect haemorrhage or alternative pathologies
  2. Carotid imaging
    • Atherosclerosis in the carotid artery may be a source of emboli in some patients
    • All patients should therefore have an urgent carotid doppler unless they are not a candidate for carotid endarterectomy
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45
Q

What is the treatment for TIA?

A

Immediate antithrombotic therapy:

  • Give aspirin 300 mg - this is for 2 weeks

Continued antithrombotic therapy after the event:

  • Clopidogrel is recommended first-line
  • Aspirin + dipyridamole given to patients who cannot tolerate clopidogrel
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46
Q

What do you give during a TIA?

A

Give aspirin 300 mg immediately, unless

  1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
  2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
  3. Aspirin is contraindicated: discuss management urgently with the specialist team
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47
Q

What is the management for a patient after a TIA if undetected at the time for before 7 and over 7 days?

A
  1. If the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis:
    • Discuss the need for admission or observation urgently with a stroke specialist
  2. If the patient has had a suspected TIA in the last 7 days:
    • Arrange urgent assessment (within 24 hours) by a specialist stroke physician
  3. If the patient has had a suspected TIA which occurred more than a week previously:
    • Refer for specialist assessment as soon as possible within 7 days
  4. Advise the person not to drive until they have been seen by a specialist.
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48
Q

What is a patient is on blood thinners and has a TIA?

A

Needs urgent CT head

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49
Q

What condition can mimic the effects of a TIA?

A

Hypoglycaemia in diabetes

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50
Q

What are the rules after a stroke or TIA for driving?

A
  1. Stroke or TIA: 1 month off driving, may not need to inform DVLA if no residual neurological deficit
  2. Multiple TIAs over short period of times: 3 months off driving and inform DVLA
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51
Q

What do midline lesions and hemisphere lesions cause in the cerebellum?

A

Midline lesions
Can produce severe gait and truncal ataxia. As they extend they can also give fourth cranial nerve lesions and severe ipsilateral arm tremor, marked nystagmus

Cerebellar hemisphere
Lesions can produce classic ipsilateral limb ataxia (intention tremor, past pointing and mild hypotonia).

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52
Q

What are the causes of cerebellar disorders?

A
  1. Vascular
    • ​​Stroke
  2. Space-occupying lesion
  3. Nutritional
    • ​​​​Thiamine
    • Vitamin E deficiency
  4. Infection
  5. Truama
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53
Q

What are the symptoms of cerebellar disorder?

A

DANISH

Dysdiadochokinesia

Ataxia (gait and posture)

Nystagmus.

Intention tremor

Scanning dysarthria

Heel-shin test positivity

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54
Q

What are the investigations for cerebellar disorder?

A

Blood tests - FBC, LFTs, cholesterol, protein electrophoresis, copper and caeruloplasmin, immunoglobulins and glycoproteins.

Electroencephalogram (EEG).

Electromyogram (EMG).

Imaging - MRI is the modality of choice.

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55
Q

What is the treatment for cerebellar disease?

A

Treat underlying condition

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56
Q

WHAT IS EPILEPSY?

A

Epilepsy is a central nervous system (neurological) disorder in which brain activity becomes abnormal, causing seizures or periods of unusual behavior, sensations, and sometimes loss of awareness.

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57
Q

What are the different types of epilepsy?

A

Focal seizures

Generalised seizures

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58
Q

What are the different focal seizures?

A

From one part of the brain

Focal seizures without loss of consciousness
Alter emotions or change the way things look, smell, feel, taste or sound. They may also result in involuntary jerking of a body part, such as an arm or leg,

Focal seizures with impaired awareness
Stare into space, repetative movements

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59
Q

What can focal seizures be further classified into?

A

Motor

  • *Non-motor**
    (e. g. déjà vu, jamais vu; )

Features such as aura

(e.g. Jacksonian march)

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60
Q

What is a Jacksonian march?

A

It characteristically starts by affecting a peripheral body part such as a toe, finger or section of the lip and then spreads quickly ‘marches’ over the respective foot, hand or face.

In some with Jacksonian march seizures (as in this case), the electrical disorder spreads over larger areas of the brain, causing the seizure to develop into a tonic-clonic seizure.

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61
Q

What are the different generalised seizures?

A

Absence seizures
Previously known as petit mal seizures. Staring into space or subtle body movements such as eye blinking or lip smacking

Tonic seizures
Tonic seizures cause stiffening of your muscles

Atonic seizures
Loss of muscle control, which may cause you to suddenly collapse or fall down.

Clonic seizures
Jerking muscle movements

Myoclonic seizures
Brief jerks or twitches of your arms and legs.

Tonic-clonic seizures
Grand mal seizures

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62
Q

What are the causes of epilepsy?

A
  1. Genetic influence
  2. Head trauma
  3. Brain conditions
    • Stroke
  4. Infectious diseases
    • Meningitis, AIDS and viral encepthalitis
  5. Prenatal injury
  6. Developmental disorders
    • Autism
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63
Q

How do you diagnose epilepsy?

A
  1. ECG 1st line
  2. MRI
  3. FBC, U+Es and glucose
  4. Brain imaging and EEG but CLINICAL DIAGNOSIS
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64
Q

What is the treatment for epilepsy?

A
  1. Generalised tonic-clonic seizures
    • Sodium valproate
    • Second line: lamotrigine, carbamazepine
  2. Focal seizures
    • Carbamazepine or lamotrigine
    • Second line: levetiracetam, oxcarbazepine or sodium valproate
  3. Absence seizures* (Petit mal)
    • Sodium valproate or ethosuximide
  4. Myoclonic seizures
    • Sodium valproate
    • Second line: clonazepam, lamotrigine
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65
Q

What are the featurs of a temporal lobe seizure?

A
  1. Hallucinations (auditory/gustatory/olfactory)
  2. Epigastric rising/Emotional
  3. Automatisms (lip smacking/grabbing of clothes/plucking)
  4. Deja vu/Dysphasia post-ictal)
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66
Q

What are the features of a frontal lobe seizure?

A
  1. Head/leg movements
  2. Posturing
  3. Post-ictal weakness
  4. Jacksonian march
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67
Q

What are the features of a parietal lobe seizure?

A

Paraesthesia

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68
Q

What are the features of an occipital lobe seizure?

A

Floaters/flashes

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69
Q

What are the features of abscence seizures?

A
  1. Absences last a few seconds and are associated with a quick recovery
  2. Seizures may be provoked by hyperventilation or stress
  3. The child is usually unaware of the seizure
  4. They may occur many times a day
  5. EEG: bilateral, symmetrical 3Hz spike and wave pattern
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70
Q

What is the management of abscence seziures?

A

Sodium valproate

Ethosuximide

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71
Q

How can you differentiate between a pseudoseizure and an epileptic seizure?

A

Prolactin levels

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72
Q

What is todd’s palsy?

A

Weakness of limbs after seizure

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73
Q

WHAT IS THE DIFFERENCE BETWEEN A VASOVAGAL AND TONIC-CLONIC SEIZURE?

A

Vasovagal shorter post-ictal

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74
Q

WHAT ARE THE FACTORS FAVOURING A NEAD?

A
  1. Pelvic thrusting
  2. Family member with epilepsy
  3. Much more common in females
  4. Crying after seizure
  5. Don’t occur when alone
  6. Gradual onset
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75
Q

What are the causes of NEAD?

A
  1. A heart condition that causes fainting
  2. Diabetes or other metabolic disorders
  3. Emotional pain
  4. Mental pain
  5. Being bullied
  6. Physical or sexual abuse
  7. A major accident
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76
Q

How do you diagnose NEAD?

A
  1. EEG
    A patient with NES will not show unusual electrical activity in the brain on the EEG.
  2. MRI + CT
    Epilepsy
  3. Blood tests
    Diabetes
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77
Q

What is the treatment for NEAD?

A

CBT

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78
Q

What should a patient tell the DVLA with epilepsy?

A

First unprovoked/isolated seizure

  1. 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG.
  2. If these conditions are not met then this is increased to 12 months

For patients with established epilepsy or those with multiple unprovoked seizures:

  1. → may qualify for a driving licence if they have been free from any seizure for 12 months
  2. → if there have been no seizures for 5 years (with medication if necessary) a ’til 70 licence is usually restored
  3. withdrawawl of epilepsy medication: should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose
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79
Q

What is narcolepsy?

A

Suddenly causes a person to fall asleep at inappropriate times

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80
Q

What is cataplexy?

A

Sudden loss of muscle tone typically triggered by emotion such as laughing or crying

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81
Q

What are the different types of narcolepsy?

A

Narcolepsy that occurs with cataplexy is called type 1 narcolepsy.

Narcolepsy that occurs without cataplexy is known as type 2 narcolepsy.

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82
Q

What is the cause of narcolepsy?

A
  1. Associated with HLA-DR2
  2. Associated with low levels of orexin (hypocretin), a protein which is responsible for controlling appetite and sleep patterns
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83
Q

What are the symptoms of narcolepsy?

A
  1. Typical onset in teenage years
  2. Hypersomnolence
  3. Cataplexy (sudden loss of muscle tone often triggered by emotion)
  4. Sleep paralysis
  5. Vivid hallucinations on going to sleep or waking up
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84
Q

How do you diagnose narcolepsy?

A

Multiple sleep latency EEG

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85
Q

What is the treatment for narcolepsy?

A

Stimulants

  1. Modafinil
  2. Armodafinil

Improves nighttime sleep

  1. Sodium oxybate
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86
Q

WHAT IS VASCULAR DEMENTIA?

A

It is not a single disease but a group of syndromes of cognitive impairment

Caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.

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87
Q

What is the cause of vascular dementia?

A

Stroke (infarction) blocking a brain artery
With both silent and apparent strokes, the risk of vascular dementia increases with the number of strokes that occur over time. One type of vascular dementia involving many strokes is called multi-infarct dementia.

Narrowed or chronically damaged brain blood vessels. These conditions include the wear and tear associated with aging, high blood pressure, abnormal aging of blood vessels (atherosclerosis), diabetes, and brain hemorrhage.

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88
Q

What are the symptoms of vascular dementia?

A
  1. Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
  2. The difficulty with attention and concentration
  3. Seizures
  4. Memory disturbance
  5. Gait disturbance
  6. Speech disturbance
  7. Emotional disturbance
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89
Q

Can vascular dementia and alzheimer’s disease occur together?

A

Yes

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90
Q

How is vascular dementia diagnosed?

A
  1. A comprehensive history and physical examination
  2. Formal screen for cognitive impairment
  3. Medical review to exclude medication cause of cognitive decline
  4. MRI scan – may show infarcts and extensive white matter changes
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91
Q

What is the treatment for vascular dementia?

A
  1. Often involves managing the risk factors
  2. Lower blood pressure
  3. Reduce your cholesterol levels
  4. Prevent your blood from clotting
  5. Help control your blood sugar
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92
Q

What is Horner’s syndrome?

A

Horner’s syndrome is a triad of features resulting from interruption of the sympathetic pathway from the hypothalamus to the orbit

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93
Q

What are the symptoms of horners syndrome?

A
  1. Miosis (small pupil)
  2. Ptosis
  3. Enophthalmos* (sunken eye)
  4. Anhidrosis (loss of sweating one side)
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94
Q

How do you diagnose horner’s syndrome?

A
  1. A normal pupil is dilated by cocaine and hydroxyamphetamine
  2. When the lesion is pre-ganglionic only hydroxyamphetamine causes dilatation
  3. When the lesion is post-ganglionic only adrenaline causes dilatation
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95
Q

What is the treatment for horners syndrome?

A

Treat underlying condition

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96
Q

What is bell’s palsy?

A

Bell’s palsy may be defined as an acute, unilateral, idiopathic,

Facial nerve paralysis

7th Nerve

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97
Q

What are the symptoms of bell’s palsy?

A
  1. Weakness to total paralysis on one side of your face — occurring within hours to days
  2. Lower motor neuron facial nerve palsy - forehead affected*
  3. Post-auricular pain (may precede paralysis)
  4. Altered taste
  5. Dry eyes
  6. Hyperacusis
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98
Q

What is the cause of bell’s palsy?

A

Latent herpes viruses (herpes simplex virus type 1 and herpes zoster virus), which are reactivated from cranial nerve ganglia

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99
Q

What is synkinesis?

A

Abnormal regrowth of nerve fibers.

This may result in involuntary contraction of certain muscles when you’re trying to move others (synkinesis)

For example, when you smile, the eye on the affected side may close.

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100
Q

How do you diagnose bell’s palsy?

A

Diagnosis of exclusion

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101
Q

What is the treatment of bell’s palsy?

A

Corticosteroids
Prednisolone

Antiviral drugs
Acyclovir

Articifical tears

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102
Q

WHAT IS BULBAR PALSY?

A

Bulbar palsy refers to a range of different signs and symptoms linked to impairment of function of the cranial nerves

IX - 9 Glossopharyngeal

X - 10 Vagus

XI - 11 Accessory

XII - 12 Hypoglossal

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103
Q

What is the cause of bulbar palsy?

A

Lower motor neuron lesion in the medulla oblongata or from lesions of the lower cranial nerves outside the brainstem

  • Vascular causes: medullary infarction
  • Degenerative diseases: amyotrophic lateral sclerosis
  • Inflammatory/infective: Guillain–Barré syndrome, poliomyelitis
  • Malignancy: brain-stem glioma, malignant meningitis
  • Toxic: botulism
  • Autoimmune: myasthenia gravis
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104
Q

What are the symptoms for bulbar palsy?

A
  1. Dysphagia (difficulty in swallowing)
  2. Difficulty in chewing
  3. Nasal regurgitation
  4. Slurring of speech
  5. Difficulty in handling secretions
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105
Q

How do you diagnose bulbar palsy?

A

EMA - electromagnetic articulography

EPG - electropalatography

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106
Q

What is the management for bulbar palsy?

A

Treat the underlying cause

Baclofen for spasticity

Anticholinergics for drooling

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107
Q

WHAT IS SHINGLES?

A

Shingles is an infection that causes a painful rash

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108
Q

What is the cause of shingles?

A

Shingles is caused by the varicella-zoster virus — the same virus that causes chickenpox

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109
Q

What are the symptoms of shingles?

A
  • Pain, burning, numbness or tingling
  • Sensitivity to touch
  • A red rash that begins a few days after the pain
  • Stripe of blisters that wraps around either the left or right side of your torso.
  • Sometimes occurs around one eye or on one side of the neck or face
  • Fluid-filled blisters that break open and crust over
  • Itching
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110
Q

How is shingles diagnosed?

A

History of pain on one side of your body

Along with the telltale rash and blisters

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111
Q

What is the treatment of shingles?

A

Acyclovir (Zovirax)

Famciclovir

Valacyclovir (Valtrex)

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112
Q

WHAT IS WERNICKE’S ENCEPHALOPATHY?

A

Lack of vitamin B-1 (thiamine)

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113
Q

What is the risk factors for Wernicke’s encephalopathy

A
  1. Inability to afford medical care and proper food
  2. Kidney dialysis, which reduces vitamin B-1 absorption
  3. AIDS, which makes you more likely to develop conditions that lead to vitamin B-1 deficiency
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114
Q

What are the causes of Wernicke’s encephalopathy?

A
  • ALCOHOL
  • Gastric bypass surgery, which makes it difficult to meet nutritional needs due to limited food portions
  • Gastric cancer, which may limit the absorption of essential nutrients
  • Colon cancer, which can result in pain that causes you to put off eating
  • Eating disorders
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115
Q

What is the classic triad which occurs in wernicke’s encephalopathy?

A
  1. Ophthalmoplegia/nystagmus
  2. Ataxia
  3. Confusion
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116
Q

What are the symptoms of Wernicke’s encephalopathy?

A
  1. Nystagmus (the most common ocular sign)
  2. Ophthalmoplegia
  3. Ataxia
  4. Confusion, altered GCS
  5. Pripheral sensory neuropathy
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117
Q

How is Wernicke’s encephalopathy diagnosed?

A
  1. Decreased red cell transketolase
  2. MRI
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118
Q

What is the treatment for Wernicke’s encephalopathy?

A
  1. Thiamine (IV vitamin B-1)
  2. Treatment for alcoholism
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119
Q

What can happen if Wernicke’s encephalopathy goes untreated?

A

Develop Korsafkoff syndrome

  1. Addition of antero- and retrograde amnnesia
  2. Confabulation
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120
Q

WHAT IS HUNTINGTONS DISEASE?

A

Huntington’s chorea is a hereditary disease that is marked by chronic, progressive chorea and marked mental deterioration in middle life, usually in the fourth decade.

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121
Q

What is the cause of Hungtington’s disease?

A

Autosomal dominant disorder

CAG repeats

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122
Q

What are the symptoms of Hungtington’s disease?

A
  1. Movement disorders
    • Involuntary jerking or writhing movements (chorea)
    • Muscle problems, such as rigidity or muscle contracture (dystonia)
  2. Cognitive disorder
    • Difficulty organizing, prioritizing or focusing on tasks
    • Lack of impulse control that can result in outbursts, acting without thinking and sexual promiscuity
  3. Psychiatric disorders
    • Feelings of irritability, sadness or apathy
    • Social withdrawal
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123
Q

How is Huntington’s disease diagnosed?

A

Neurological examination
Motor symptoms, such as reflexes, muscle strength and balance
Sensory symptoms, including sense of touch, vision and hearing
Psychiatric symptoms, such as mood and mental status

Brain imaging

Genetic testing

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124
Q

What is the treatment for Huntington’s disease?

A

Control movement

  1. Tetrabenazine
  2. Deutetrabenazine

Antipsychotic drugs

  1. Haloperidol
  2. Fluphenazine

Antidepressants

  1. Citalopram

Psychotherapy

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125
Q

WHAT IS PARKINSON’S DISEASE?

A

Parkinson’s disease is a condition in which parts of the brain become progressively damaged over many years

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126
Q

What is the cause of Parkinson’s disease?

A

Lack of dopamine

Exact cause is unknown

Due to genetic factors and environmental triggers

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127
Q

What are the symptoms of Parkinson’s disease?

A
  1. Tremor
    • unilateral tremor that improves with voluntary movement
  2. Bradykinesia
  3. Rigid muscles
  4. Impaired posture and balance
  5. Loss of automatic movements
  6. Speech changes
  7. Writing changes
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128
Q

How do you diagnose Parkinson’s disease?

A
  1. Mainly clinical
  2. Can do a SPECT scan
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129
Q

What are the causes of parkinsonism?

A
  1. Progressive supranuclear palsy
  2. Multiple system atrophy
  3. Drug-induced e.g. antipsychotics, metoclopramide*
  4. Wilson’s disease
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130
Q

What is the treatment for Parkinson’s disease?

A
  1. If symptoms are affecting quality of life then levodopa first
  2. If not affecting quality of life then dopamine agonist or MOA

Medications

  1. Dopamine agonists
    • Ropinirole, cabergoline, pramipexole - Associated with inhibition
  2. MAO B inhibitors
    • ​​Selegiline, rasagiline
      Prevent the breakdown of dopamine
  3. Catechol O-methyltransferase (COMT) inhibitors
    • ​​Entacapone
      Blocks an enzyme that breaks down dopamine
  4. Carbidopa-levodopa

Deep brain stimulation

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131
Q

Impulse control disorders are associated with what part of parkinsons?

A
  1. Dopamine agonist therapy
  2. A history of previous impulsive behaviours
  3. A history of alcohol consumption and/or smoking
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132
Q

What drugs can worsen symptoms in parkinson’s disease?

A

Haloperidol

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133
Q

What drug use useful for managing tremor in drug-induced parkinsonism?

A

Ropinirole

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134
Q

What food should you avoid when taking a monoamine oxidase inhibitor?

A

Cheese

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135
Q

WHAT IS ALZHEIMER’S DISEASE?

A

Most common cause of dementia

Causes the brain cells to degenerate and die

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136
Q

What causes alzheimer’s disease?

A

Exact cause is unknown

Brain proterins fail to function properly, disrupt brain neurons and unleash a series of toxic events

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137
Q

What are the two proteins involved with alzheimers disease?

A

Plaques
Beta-amyloid is a leftover fragment of a larger protein. When these fragments cluster together, they appear to have a toxic effect on neurons and to disrupt cell-to-cell communication. These clusters form larger deposits called amyloid plaques, which also include other cellular debris.

Tangles
Tau proteins play a part in a neuron’s internal support and transport system to carry nutrients and other essential materials. In Alzheimer’s disease, tau proteins change shape and organize themselves into structures called neurofibrillary tangles. The tangles disrupt the transport system and are toxic to cells

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138
Q

What are the symptoms of alzheimer’s disease?

A
  1. Memory
    • ​​Early sign of the disease, difficulty remembering recent events
  2. Thinking and reasoning
  3. Making judgements and decisions
  4. Planning and performing familiar tasks
  5. Changes in personality and behaviour
  6. Preserved skills
    • ​​Reading or listening to books
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139
Q

What are the risk factors for developing alzheimer’s disease?

A

Age

Family history and genetics
Apolipoprotein E gene (APOE)

Down syndrome
Three copies of chromosome 21, appear 10 to 20 years earlier

Woman
Live longer than men

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140
Q

How do you diagnose alzheimer’s disease?

A
  1. Brain imaging - MRI/CT
    • Widespread cerebral atrophy, particulary the coretex and hippocampus
    • Cortical plaques due to depositiuon of type A-beta-amyloid protein and intraneuronal neurofibriallry tau tangles
  2. ​​​Lab tests
    • ​​Thyroid disorders or vitamin deficiencies
    • Deficit of acetylcholine from damage to ascending forebrain projection
  3. PET
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141
Q

What is the treatment for alzheimer’s disease?

A

Treat cognitive symptoms

  • Cholinesterase inhibitors - preserve acetylcholine
  • *Donepezil, galantamine, rivastigmine**
  • N-methyl-d-aspartate (NMDA) inhibitor - glutamate
  • *Memantine**

Safe environment

Alternative medicine

  • Omega-3 fatty acids
  • Curcumin
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142
Q

WHAT IS FRONTOTEMPORAL LOBAR DEGENERATION?

A

Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia

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143
Q

What are the different types of frontotemporal lobar degeneration?

A
  1. Frontotemporal dementia (Pick’s disease)
  2. Progressive non fluent aphasia (chronic progressive aphasia, CPA)
  3. Semantic dementia
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144
Q

What are the factors that favour frontotemporal lobar dementias?

A
  1. Onset before 65
  2. Insidious onset
  3. Relatively preserved memory and visuospatial skills
  4. Personality change and social conduct problems
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145
Q

What are the features of pick’s disease?

A
  1. Personality change and impaired social conduct.

Other common features include

  1. Hyperorality
  2. Disinhibition
  3. Uncreased appetite
  4. Perseveration behaviours
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146
Q

What are the investigations for pick’s disease?

A
  1. Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.
  2. Macroscopic changes seen in Pick’s disease include:-
    • Atrophy of the frontal and temporal lobes
  3. Microscopic changes include:-
    • Pick bodies - spherical aggregations of tau protein (silver-staining)
    • Gliosis
    • Neurofibrillary tangles
    • Senile plaques
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147
Q

What is the treatment of pick’s disease?

A
  1. NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia
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148
Q

WHAT IS NORMAL PRESSURE HYDROCEPHALUS?

A

Excess cerebrospinal fluid accumulates in the ventricles

Called “normal pressure” because despite the excess fluid, CSF pressure as measured during a spinal tap is often normal.

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149
Q

What is the cause of normal pressure hydrocephalus?

A

Tumor, head injury, hemorrhage, infection or inflammation

In most cases, the cause of the fluid buildup remains unknown

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150
Q

What are the symptoms of normal pressure hydrocephalus?

A
  1. Difficulty walking
  2. Mild dementia
  3. Decline in thinking skills
  4. Loss of bladder control
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151
Q

How do you diagnose normal pressure hydrocephalus?

A

Brain imaging
Enlargement of the ventricles

Lumbar puncture
CSF normal or intermittently raised

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152
Q

What is the treatment for normal pressure hydrocephalus?

A

Ventriculoperitoneal shunting

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153
Q

What is hydrocephalus?

A

Hydrocephalus is the buildup of fluid in the cavities (ventricles) deep within the brain

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154
Q

What is the cause of hydrocephalus?

A

Hydrocephalus is caused by an imbalance between how much cerebrospinal fluid is produced and how much is absorbed into the bloodstream

Obstruction

Poor absorption

Overproduction

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155
Q

What are the symptoms of hydrocephalus?

A

Patients with hydrocephalus present with symptoms due to raised intracranial pressure, which include:

  1. Headache (typically worse in the morning, when lying down and during valsalva)
  2. Nausea and vomiting
  3. Papilloedema
  4. Coma (in severe cases)
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156
Q

How do you diagnose hydrocephalus?

A
  1. CT head - first line
  2. MRI
    • May be used to investigate hydrocephalus in more detail
  3. Lumbar puncture*
    • Is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure
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157
Q

What is the treatment for hydrocephalus?

A
  1. An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  2. A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum
  3. In obstructive hydrocephalus, the treatment may involve surgically treating the obstructing pathology
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158
Q

What are the most common places for cancer to metastisise to the brain?

A
  • Lung (most common)
  • Breast
  • Bowel
  • Skin (namely melanoma)
  • Kidney
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159
Q

What is the most common brain cancer in adults?

A

Glioblastoma multiforme

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160
Q

What can be used to treat oedema caused from a gliblastoma multiforme?

A

Dexamethosone

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161
Q

What is the most common peadiatric brain cancer?

A

Pilocytic astrocytoma

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162
Q

What is multiple sclerosis?

A

Inflammatory, demyelinating disease.

Specific to the central nervous system.

Has relapsing and remitting symtptoms.

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163
Q

What is the cause of multiple sclerosis?

A
  1. Vit D deficiency
  2. Genetics
    • Female
    • HLA DR2
  3. Environment
    • Infections
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164
Q

What are the symptoms of multiple sclerosis?

A
  1. Optic neuritis (impaired vision and eye pain)
  2. Nystagmus, double vision and vertigo
  3. Bladder and sexual dysfunction
  4. Spasticity and other pyramidal signs
  5. Sensory symptoms and signs
  • Reduced visual acuity after exercise = Uhthoff’s phenomenon
  • Lhermitte’s sign (electric shock-like sensation that occurs on flexion of the neck.)
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165
Q

How do you diagnose multiple sclerosis?

A
  1. CONTRAST MRI
    • High signal T2 lesions
    • Periventricular plaques
    • Dawson fingers
  2. CSF
    • Oligoclonal bands (and not in serum)
    • Increased intrathecal synthesis of IgG
  3. Visual evoked potentials
    • Delayed, but well preserved waveform
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166
Q

What is the diagnostic criteria for MS?

A

Two or more CNS lesions disseminated in time and space

Exclusion of conditions giving a similar clinical picture

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167
Q

What is the treatment for multiple sclerosis?

A
  1. Treatment to modify progression
    • Primary-progressive - ocrelizumab
  2. For MS attacks
    • Oral or IV Methylpredisolone for 5 days
    • Plasmapheresis
168
Q

What is guillian-Barre syndrome?

A

Guillain-Barre syndrome describes an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni).

169
Q

What is the cause of guillian-barre?

A
  1. The exact cause of Guillain-Barre syndrome isn’t known.
  2. The disorder usually appears days or weeks after a respiratory or digestive tract infection
  3. Classically Campylobacter jejuni
170
Q

What are the symptoms of guillian-bare?

A

Progressive, symmetrical weakness of all the limbs

  1. The weakness is classically ascending i.e. the legs are affected first
  2. Reflexes are reduced or absent
  3. Sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs
171
Q

How is guillain-barre diagnosed?

A
  1. Lumbar puncture
    • Rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
  2. Nerve condution studies may be performed
    • Decreased motor nerve conduction velocity (due to demyelination)
    • Prolonged distal motor latency
    • Increased F wave latency
172
Q

What is the treatment for guillian-barre syndrome?

A
  1. Plasma exchange
  2. Immunoglobulin therapy
173
Q

What is motor neuron disease?

A

Motor neurone disease (MND) is a neurodegenerative condition that affects the brain and spinal cord. MND is characterised by the degeneration of primarily motor neurones, leading to muscle weakness.

174
Q

What are ther symptoms of motor neuron disease?

A

Clues which point towards motor neuron disease:

  1. Fasciculations
  2. The absence of sensory signs/symptoms*
  3. The mixture of lower motor neuron and upper motor neuron signs
  4. Wasting of the small hand muscles/tibialis anterior is common

Other features

  1. Doesn’t affect external ocular muscles
  2. No cerebellar signs
  3. Abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
175
Q

How do you diagnose MND?

A

Nerve conduction studies
Normal motor conduction and can help exclude a neuropathy.

Electromyography
Reduced number of action potentials with increased amplitude.

MRI
Exclude the differential diagnosis of cervical cord compression and myelopathy

176
Q

What is the management for motor neuron disease?

A

Riluzole
Prevents stimulation of glutamate receptors
Used mainly in amyotrophic lateral sclerosis
Prolongs life by about 3 months

Respiratory care
Non-invasive ventilation (usually BIPAP) is used at night
Studies have shown a survival benefit of around 7 months

177
Q

What does the oxford stroke classification classify strokes based on?

A
  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction e.g. dysphasia
178
Q

What does total anterior circulaion infarcts involve within the oxford stroke classification?

A

Involves middle and anterior cerebral arteries

  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction e.g. dysphasia
179
Q

What does partial anterior circulation infarct involve within the oxford stroke classification?

A

Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction e.g. dysphasia

2 of the above criteria are present

180
Q

What is a lacunar infarct?

A

Involves perforating arteries around the internal capsule, thalamus and basal ganglia

181
Q

What do lacunar infarcts present with?

A

Presents with 1 of the following:

  1. Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three
  2. Pure sensory stroke
  3. Ataxic hemiparesis
182
Q

What do posterior circulation infarcts involve?

A

Involves vertebrobasilar arteries

183
Q

What do posterior circulation infarcts present with?

A

Presents with 1 of the following:

  1. SIGHT - Isolated homonymous hemianopia
  2. MOVEMENT - Cerebellar or brainstem syndromes
  3. Loss of consciousness
184
Q

What does lateral medullary syndrome (posterior inferior cerebellar artery) present with?

A
  1. Ipsilateral:
    • Ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  2. Contralateral:
    • Limb sensory loss
185
Q

What is weber’s syndrome?

A
  1. Ipsilateral III palsy (closed eyelid and eye outward and down)
  2. Contralateral weakness
186
Q

WHAT IS TUBEROUS SCLEROSIS?

A

Genetic condition that causes mainly non-cancerous (benign) tumours to develop in different parts of the body.

187
Q

What is the cause of tuberous sclerosis?

A

Autosomal dominant

188
Q

How do you diagnose tuberous sclerosis?

A

Wood’s light
Ultraviolet used to reveal hypopigmented patches on skin

CT or MRI
Detect tubers and calcification

Echocardiography
If any cardiac rhabdomyomas are suspected

189
Q

What are the symptoms of tuberous sclerosis?

A

Cutaneous features

  1. Depigmented ‘ash-leaf’ spots which fluoresce under UV light
  2. Roughened skin over lumbar spine (Shagreen patches)
  3. Adenoma sebaceum (angiofibromas): butterfly distribution over nose
  4. Fibromata beneath nails (subungual fibromata)
  5. Café-au-lait spots* may be seen

Neurological features

  1. Developmental delay
  2. Epilepsy (infantile spasms or partial)
  3. Intellectual impairment

Retinal hamartomas: dense white areas on retina (phakomata)

190
Q

What is the treatment for tuberous sclerosis?

A

Medications
Anti-seizure

Surgery
Remove organs

191
Q

What is sleep paralysis?

A

Sleep paralysis is when you cannot move or speak as you are waking up or falling asleep. It can be scary but it’s harmless and most people will only get it once or twice in their life

192
Q

What are the symptoms of sleep paralysis?

A

Paralysis
This occurs after waking up or shortly before falling asleep

Hallucinations
Images or speaking that appear during the paralysis

193
Q

What are the causes of sleep paralysis?

A
  1. Insomnia
  2. Disrupted sleeping patterns – for example, because of shift work or jet lag
  3. Narcolepsy – a long-term condition that causes a person to suddenly fall asleep
  4. General anxiety disorder
  5. Panic disorder
194
Q

What is the management of sleep paralysis?

A

Clonazepam

195
Q

What does the third nerve do?

A
  1. The third cranial nerve controls the movement of four of the six eye muscles.
  2. These muscles move the eye inward, up and down, and they control torsion (rotating the eye downward and toward the ear on the same side)
  3. The third cranial nerve also controls constriction of the pupil, the position of the upper eyelid, and the ability of the eye to focus
196
Q

What are the causes of third nerve palsys?

A
  1. Diabetes mellitus
  2. Vasculitis e.g. temporal arteritis, SLE
  3. Posterior communicating artery aneurysm
  4. Cavernous sinus thrombosis
  5. Weber’s syndrome: ipsilateral third nerve palsy with contralateral hemiplegia -caused by midbrain strokes
197
Q

What are the symptoms of a third nerve palsy?

A

Eye is deviated ‘down and out’

Ptosis

Pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

198
Q

What are the symptoms of a fourth nerve palsy?

A

Palsy results in defective downward gaze → vertical diplopia

199
Q

What are the symptoms of sixth nerve palsy?

A

Palsy results in defective abduction → horizontal diplopia

200
Q

What is the treatment of a third nerve palsy?

A

Relief of pressure on the third nerve from a tumor or blood vessel (aneurysm) with surgery may improve the third nerve palsy.

201
Q

What is myasthenia gravis?

A

Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors.

Antibodies to acetylcholine receptors are seen in 85-90% of cases

202
Q

What is the causes of myasthenia gravis?

A
  1. Antibodies that attack acetylcholine receptors
  2. Thymus gland maintains the production of these
203
Q

Who is myasthenia gravis more common in?

A

Women

204
Q

What are the symptoms of myasthenia gravis?

A
  1. Progressive weakness with movement
  2. Extraocular muscle weakness
    • ​​Diplopia
  3. Proximal muscle weakness
    • Face, neck, limb girdle
  4. Ptosis
  5. Dysphagia
205
Q

What is myasthenia gravis associated with?

A
  1. Thymomas in 15%
  2. Thymic hyperplasia in 50-70%
  3. Autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
206
Q

How is myasthenia gravis diagnosed?

A
  1. Single fibre electromyography
    • High sensitivity (92-100%)
  2. CT thorax to exclude thymoma
  3. CK normal
  4. Autoantibodies - DIAGNOSIS
    • 85-90% of patients antibodies to acetylcholine receptors. In the remaining patients, 40% positive for anti-muscle-specific tyrosine kinase antibodies
  5. Tensilon test
    • IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia
207
Q

What are the exaccerbating factors for myasthenia gravis?

A
  1. Penicillamine
  2. Quinidine, procainamide
  3. Beta-blockers
  4. Lithium
  5. Phenytoin
  6. Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
208
Q

What is the treatment for myastenia gravis?

A
  1. Long-acting acetylcholinesterase inhibitors
    • Pyridostigmine is first-line
  2. Immunosuppression
    • Prednisolone initially
    • Azathioprine, cyclosporine, mycophenolate mofetil may also be used
  3. Thymectomy
209
Q

What is a myasthenic crisis?

A

Myasthenic crisis is a life-threatening complication of myasthenia gravis.

It’s when the muscles that you use to breathe get so weak that you can’t get air in and out of your lungs.

210
Q

What are some causes of a myasthenic crisis?

A
  1. Non-compliance with medication
  2. Excessive activity
  3. Infection
  4. Drugs
    Penicillamine
    Beta-blockers
    Lithium
    Phenytoin
    Antibiotics: gentamicin, macrolides, quinolones, tetracyclines
211
Q

What are the symptoms of a myasthenic crisis?

A

Laboured shallow breathing

212
Q

What is the management of myasthenic crisis?

A
  1. Plasmapheresis
  2. IVIg
213
Q

WHAT IS LAMBERT-EATON SYNDROME?

A

Lambert-Eaton myasthenic syndrome is seen in association with small cell lung cancerand to a lesser extent breast and ovarian cancer. It may also occur independently as an autoimmune disorder. Lambert-Eaton myasthenic syndrome is caused by an antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.

214
Q

What are the features of Lambert-Eaton syndrome?

A
  1. repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
  2. in reality, this is seen in only 50% of patients and following prolonged muscle use muscle strength will eventually decrease
  3. limb-girdle weakness (affects lower limbs first)
  4. hyporeflexia
  5. autonomic symptoms: dry mouth, impotence, difficulty micturating
  6. ophthalmoplegia and ptosis not commonly a feature (unlike in myasthenia gravis)
215
Q

What are the investigations for Lambert-Eaton syndrome?

A

incremental response to repetitive electrical stimulation

216
Q

What is the management for Lambert-Eaton syndrome?

A
  1. Treatment of underlying cancer
  2. Immunosuppression, for example with prednisolone and/or azathioprine
  3. 3,4-diaminopyridine is currently being trialled
    • Works by blocking potassium channel efflux in the nerve terminal so that the action potential duration is increased. Calcium channels can then be open for a longer time and allow greater acetylcholine release to the stimulate muscle at the end plate
  4. Intravenous immunoglobulin therapy and plasma exchange may be beneficial
217
Q

Where is the lesion for a bitemporal hemionopia?

A

Optic chiasm

218
Q

What does congrous and incongrous mean?

A

A congruous defect is complete or symmetrical visual field loss

Incongruous defect is incomplete or asymmetric

219
Q

What is the cause of a bitemproal hemionopia?

A

Upper quadrant defect > lower quadrant defect =
Inferior chiasmal compression, commonly a pituitary tumour

Lower quadrant defect > upper quadrant defect =
Superior chiasmal compression, commonly a craniopharyngioma

220
Q

Where is the lesion for a homonymous hemianopia?

A
  1. Incongruous defects: lesion of optic tract
  2. congruous defects: lesion of optic radiation or occipital cortex
  3. macula sparing: lesion of occipital cortex
221
Q

Where is the lesion for a homonymous quadrantanopias?

A

Superior: lesion of temporal lobe

Inferior: lesion of parietal lobe

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

222
Q

What are the dermotomes of the body?

A
223
Q

What are the myotomes of the body?

A

A myotome is a group of muscles innervated by the ventral root a single spinal nerve

224
Q

What should an individual tell the DVLA after scncope?

A
  1. Simple faint: no restriction
  2. Single episode, explained and treated: 4 weeks off
  3. Single episode, unexplained: 6 months off
  4. Two or more episodes: 12 months off
225
Q

What is status epilepticus?

A
  1. A single seizure lasting >5 minutes, or
  2. >= 2 seizures within a 5-minute period without the person returning to normal between them
226
Q

What are some causes of status epilepticus?

A
  1. RULE OUT HYPOXIA AND GLUCOSE FIRST
  2. Stroke
  3. Imbalance of substances in the blood, such as low blood sugar
  4. Drinking too much alcohol or having alcohol withdrawal after previous heavy alcohol use
227
Q

What are the symptoms of status epilepticus?

A
  1. Muscle spasms
  2. Falling
  3. Confusion
  4. Unusual noises
  5. Loss of bowel or bladder control
  6. Clenched teeth
  7. Irregular breathing
  8. Unusual behavior
  9. Difficulty speaking
  10. A “daydreaming” look
228
Q

How do you diagnose status epilepticus?

A

EEG

Spinal Tap

229
Q

What is the management for status epilepticus?

A
  1. ABC
    • ​​Oxygen
    • Check Blood Glucose
  2. PR Benzodiazepams Prehospital - IV if in hospital
    • PR Diazepam or
    • IV lorazepam (can be repeated once after 10-20 minutes)
  3. If prolonged
    • ​​Phenytoin
    • General anaesthetic
230
Q

What what level of the spinal cord does autonomic dysreflexia happen below?

A

T6

231
Q

What do the different types of brain haemorrhages look like on imaging?

A
232
Q

What is trigeminal neuralgia?

A

Pain syndrome characterised by severe unilateral pain

233
Q

What are the red flag symptoms for trigeminal neuralgia?

A
  1. Sensory changes
  2. Deafness or other ear problems
  3. History of skin or oral lesions that could spread perineurally
  4. Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  5. Optic neuritis
  6. A family history of multiple sclerosis
  7. Age of onset before 40 years
234
Q

What is the cause of trigeminal neuralgia?

A

The vast majority of cases are idiopathic but compression of the trigeminal roots by tumours or vascular problems may occur.

235
Q

How do you diagnose trigeminal neuralgia?

A
  1. Type
  2. Pain
  3. Triggers
    • Eating, talking or even encountering a cool breeze.
236
Q

What is the management for trigeminal neuralgia?

A
  1. Carbamazepine is first-line
  2. failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
237
Q

What is neurofibromatosis?

A

Neurofibromatosis is a genetic disorder that causes tumors to form on nerve tissue

238
Q

What are the different types of neurofibromatosis?

A

NF1 and NF2
Autosomal dominant

NF1 is also known as von Recklinghausen’s syndrome.
Chromosome 17

NF2
Chromosome 22

239
Q

What are the differences between type 1 and type 2 neurofibromatosis?

A

NF1

  1. Café-au-lait spots
  2. Axillary/groin freckles
  3. Peripheral neurofibromas
  4. Iris hamatomas (Lisch nodules)in > 90%
  5. Scoliosis
  6. Pheochromocytomas

NF2

  1. Bilateral vestibular schwannomas
  2. Multiple intracranial schwannomas, mengiomas and ependymomas
240
Q

How do you diagnose neurofibromatosis?

A
  1. >6 cafe au lait spots
  2. Eye exam
  3. Hearing and balance exam
  4. Imaging
  5. Genetic testing
241
Q

What is the treatment for neurofibromatosis?

A
  1. Monitor
  2. Surgery to remove tumours
  3. Stereotactic surgery
  4. Cochlear implants
242
Q

What is the difference between neurofibromatosis vs tuberous sclerosis?

A
243
Q

WHAT ARE THE SYMPTOMS OF A VESTIBULAR SCWANNOMA?

A
  1. Vertigo
  2. Hearing loss
  3. Tinnitus
  4. Absent corneal reflex
244
Q

What is the imaging of choice for a vestibular schwannoma?

A
  1. Gadolinium-enhanced MRI of the cerebellopontine angle is the investigation of choice.
  2. Audiometry is also important as only 5% of patients will have a normal audiogram.
245
Q

What are the symptoms of cerebellar disease?

A

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’

A - Ataxia (limb, truncal)

N - Nystamus (horizontal = ipsilateral hemisphere)

I - Intention tremour

S - Slurred staccato speech, Scanning dysarthria

H - Hypotonia

246
Q

What are the causes of cerebellar disease?

A
  1. Friedreich’s ataxia, ataxic telangiectasia
  2. Neoplastic: cerebellar haemangioma
  3. Stroke
  4. Alcohol
  5. Multiple sclerosis
  6. Hypothyroidism
  7. Drugs: phenytoin, lead poisoning
  8. Paraneoplastic e.g. secondary to lung cancer
247
Q

What is a peripheral neuropathy?

A

A result of damage to the nerves outside of the brain and spinal cord (peripheral nerves)

248
Q

Which peripheral neuropathies are predominantly motor loss?

A
  • Guillain-Barre syndrome
  • Diphtheria
  • Lead poisoning
  • Hereditary sensorimotor neuropathies (HSMN)
  • Charcot-Marie-Tooth
  • Porphyria
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
249
Q

What peripheral neuropathies are predominantly sensory loss?

A
  1. Diabetes
  2. Vitamin B12 deficiency
  3. Alcoholism
  4. Amyloidosis
  5. Leprosy
250
Q

What are nerve root does the bicep reflex?

A

C5-C6

251
Q

What are the nerve roots that are responsible for the tricep reflex?

A

C7-C8

252
Q

WHAT IS MENINGITIS?

A

Inflammation of the meningies lining the brain

253
Q

What are the symptoms of meningitis?

A
  1. Sudden high fever
  2. Stiff neck
  3. Severe headache that seems different from normal
  4. Headache with nausea or vomiting
  5. Confusion or difficulty concentrating
  6. Seizures
  7. Sleepiness or difficulty waking
  8. Sensitivity to light
  9. No appetite or thirst
  10. Skin rash (sometimes, such as in meningococcal meningitis)
254
Q

What bacteria cause meningitis?

A

0 - 3 months

  • Group B Streptococcus (most common cause in neonates)
  • E. coli
  • Listeria monocytogenes

3 months - 6 years

  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Haemophilus influenzae

6 years - 60 years

  • Neisseria meningitidis
  • Streptococcus pneumoniae
255
Q

What viruses cause meningitis?

A
  1. Herpes simplex virus
  2. HIV
  3. Mumps virus
256
Q

What are the fungal causes of meningitis?

What stain is used to detect this?

A

Cryptococcal meningitis

India ink

257
Q

What are the complications of meningitis?

A
  1. Sensorineural hearing loss (most common)
  2. Seizures
  3. Focal neurological deficit
  4. Infective
    • Sepsis
    • Intracerebral abscess
  5. pressure
    • Brain herniation
    • Hydrocephalus
258
Q

How do you diagnose meningitis?

A
  1. Full blood count
  2. CRP
  3. Coagulation screen
  4. Blood culture
  5. Whole-blood PCR
  6. Blood glucose
  7. Blood gas
  8. Lumbar puncture if no signs of raised intracranial pressure
259
Q

What is the treatment of meningitis?

A
  1. IM Benzylpenicillin
    at GP
  2. Antibiotics
    < 3 months: IV amoxicillin + IV cefotaxime
    > 3 months: IV cefotaxime
  3. Steroids
    Dexamethasone
  4. Give contacts some prophylaxis
    Ciprofloxacin
    Rifampicin
260
Q

What are the different components of bacteria, viral, TB and fungal meningitis?

Appearance

Glucose

Protein

White Cells

A
261
Q

WHAT IS THE GLASGOW COMA SCORE?

A

Describe the level of consciousness in a person following a traumatic brain injury

262
Q

What drug is given to close contacts with meningitis?

A

Rifampicin OR Ciprofloxacin within 7 days of contact

263
Q

What are the different parts of the GCS?

A

Motor response - 6

Verbal reponse - 5

Eye opening response - 4

264
Q

What points are given for each motor response in GCS?

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Flexion
  5. Extension
  6. None
265
Q

What points are given to verbal response in GCS?

A

5 - Orientated
4 - Confused
3 - Words
2. - Sounds
1 - None

266
Q

What points are given to eye opening in GCS?

A
  • 4 - Spontaneous
  • 3 - To speech
  • 2 - To pain
  • 1 - None
267
Q

Below what GCS score do you intubate?

A

Below 8

268
Q

What is the Romberg’s test?

A

Test used in an exam of neurological function for balance, and also as a test for driving under the influence of an intoxican

269
Q

What is the Jendrassik maneuver?

A

Patient clenches the teeth, flexes both sets of fingers into a hook-like form, and interlocks those sets of fingers together.

The tendon below the patient’s knee is then hit with a reflex hammer to elicit the patellar reflex.

270
Q

What is the Hoffmann’s sign?

A
  1. Involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down
  2. A positive Hoffmann’s sign is suggestive of corticospinal tract dysfunction localized to the cervical segments of the spinal cord
  3. In this regard, it is analogous to the Babinski sign.
271
Q

What is the hoover’s sign?

A

The purpose of the test is to distinguish between leg paresis that is psychogenic from that which is genuine.

272
Q

What is an extradural haematoma?

A

An extradural (or ‘epidural’) haematoma is a collection of blood that is between the skull and the dura

273
Q

What is normally the cause of an extradural haemotoma?

A

It is almost always caused by trauma and most typically by ‘low-impact’ trauma (e.g. a blow to the head or a fall).

274
Q

What artery is affected in an extradural haemotoma?

A

Middle meningeal artery

275
Q

What are the symptoms of the extradural haemotoma?

A
  1. ‘Lucid interval’
  2. This is lost eventually due to the expanding haematoma and brain herniation.
  3. As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli and the patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve.
276
Q

What is seen on a CT in extradural haemotoma?

A

Biconvex (or lentiform), hyperdense collection around the surface of the brain. They are limited by the suture lines of the skull.

277
Q

What is the treatment for an extradural haemotoma?

A

Craniotomy and evacuation of the haematoma

278
Q

What is a subdural haematoma?

A

A subdural haematoma is a collection of blood deep to the dural layer of the meninges.

The blood is not within the substance of the brain and is therefore called an ‘extra-axial’ or ‘extrinsic’ lesion.

They can be unilateral or bilateral.

279
Q

How will an acute subdural haematoma look on CT?

A
  1. CT imaging is the first-line investigation and will show a crescentic collection, not limited by suture lines.
  2. They will appear hyperdense (bright) in comparison to the brain.
  3. Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation.
280
Q

What is the management for an acute subdural haematoma?

A

Small or incidental acute subdurals can be observed conservatively.

Surgical options include monitoring of intracranial pressure and decompressive craniectomy.

281
Q

What is the cause of a chronic subdural haematoma?

A

Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding.

Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taut bridging veins.

Infants also have fragile bridging veins and can rupture in shaken baby syndrome.

282
Q

What do chronic subdural haematomas look like on CT?

A

On CT imaging they similarly are crescentic in shape, not restricted by suture lines and compress the brain (‘mass effect’).

In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain.

283
Q

What is the management of a chronic subdural haematoma?

A
  1. Conservative

OR

  1. If the patient is confused, has an associated neurological deficit or has severe imaging findings then surgical decompression with burr holes is required.
284
Q

What is Wernicke’s (receptive) aphasia?

A

The ability to grasp the meaning of spoken words and sentences is impaired, while the ease of producing connected speech is not very affected.

herefore Wernicke’s aphasia is also referred to as ‘fluent aphasia’ or ‘receptive aphasia’.

Comprehension is impaired

285
Q

Where is the lesion for wernicke’s aphasia?

A

Superior temporal gyrus

It is typically supplied by the inferior division of the left middle cerebral artery

286
Q

What is Broca’s (expressive) aphasia?

A

Partial loss of the ability to produce language (spoken, manual, or written)

A person with expressive aphasia will exhibit effortful speech.

Comprehension is normal

287
Q

Where is the lesion in broca’s aphasia?

A

Due to a lesion of the inferior frontal gyrus.

It is typically supplied by the superior division of the left MCA

288
Q

What are the symptoms of conduction aphasia?

A

Speech fluent, repetition poor

289
Q

What are the side effects of sodium valporate?

A

P450 inhibitor

  1. Gastrointestinal: nausea
  2. Increased appetite and weight gain
  3. Alopecia: regrowth may be curly
  4. Ataxia
  5. Tremor
  6. Hepatotoxicity
  7. Pancreatitis
  8. Thrombocytopaenia
  9. Teratogenic
  10. Hyponatraemia
290
Q

What is the treatment for neuropathic pain?

A
  1. Amitriptyline
  2. Duloxetine
  3. Gabapentin
  4. Pregabalin

if the first-line drug treatment does not work try one of the other 3 drugs

  1. Tramadol
    Rescue therapy
291
Q

What are the side effects of levo-dopa?

A
  • Dyskinesia
  • ‘on-off’ effect
  • Postural hypotension
  • Cardiac arrhythmias
  • Nausea & vomiting
  • Psychosis
  • Reddish discolouration of urine upon standing
292
Q

What is the recognition of Stroke in the Emergency Room scale used for?

A

Effective in the initial differentiation of acute stroke from stroke mimics.

293
Q

What are the red flags for headaches?

A
  1. Compromised immunity
  2. Age under 20 years and a history of malignancy
  3. A history of malignancy known to metastasis to the brain
  4. Vomiting without other obvious cause
  5. Worsening headache with fever
  6. Sudden-onset headache reaching maximum intensity within 5 minutes - ‘thunderclap’
  7. New-onset cognitive dysfunction
  8. Change in personality
  9. Headache triggered by cough, valsalva (trying to breathe out with nose and mouth blocked), sneeze or exercise
  10. Orthostatic headache (headache that changes with posture)
294
Q

What are the contraindications for triptan use?

A
  1. Ischaemic heart disease
  2. Cerebrovascular disease
    • E.g Stroke, aneurysm
295
Q

What is idiopathic intracranial hypertension?

A

Pseuodtumour cerebri describes raised intracranial pressure in the absence of a mass lesion or of hydrocephalus

296
Q

What are the risk factors for idiopathic intracranial hypertension?

A
  1. Fat
  2. Famle
  3. Forty
  4. Pregnancy

Drugs*: oral contraceptive pill, steroids, tetracycline, vitamin A, lithium

297
Q

What are the features of idiopathic intracranial hypertension?

A
  1. Headache
  2. Blurred vision
  3. Papilloedema (usually present)
  4. Enlarged blind spot
  5. Sixth nerve palsy may be present
298
Q

What is the management of idiopathic intracranial hypertension?

A
  1. Weight loss
  2. Diuretics
    • e.g. acetazolamide
  3. Topiramate (anti-convulsant) is also used, and has the added benefit of causing weight loss in most patients
  4. Repeated lumbar puncture
  5. Surgery
    • ​​​Optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve.
    • A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
299
Q

WHAT ARE THE FEATURES OF ENCEPHALITIS?

A
  1. Fever, headache, psychiatric symptoms, seizures, vomiting
  2. Focal features e.g. aphasia
  3. Peripheral lesions (e.g. cold sores) have no relation to presence of HSV encephalitis
300
Q

What is the cause of encephalitis?

A

HSV-1 responsible for 95% of cases in adults

Typically affects temporal and inferior frontal lobes

301
Q

What are the investigations for encephalitis?

A
  1. CSF
    • Lymphocytosis, elevated protein
    • PCR for HSV
  2. CT
    • Medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
    • LOW DENSITY
  3. Note - MRI is better
  4. EEG pattern
    • Lateralised periodic discharges at 2 Hz
302
Q

What is the management of encephalitis?

A

IV aciclovir

303
Q

What is given to reduce the effects of heparin?

A

Protamine sulphate

304
Q

What is given to reverse the effects of DOACs?

A

Beriplex

305
Q

What is given to reverse the effects of warfarin?

A

Vitamin K

306
Q

WHAT IS A SQUINT?

A

A squint is a condition in which the visual axes of each eye are not directed simultaneously at the same object.

307
Q

What are the investigations for a squint?

A
  1. Facial appearance
  2. Corneal reflections - symmetrical on pupil
  3. Head tilt
  4. Test ocular movements
  5. Cover test
308
Q

What is the management of a squint?

A
  1. Referral to secondary care
  2. Eye patches can be useful to prevent ambylopia
309
Q

WHAT IS CEREBRAL PALSY?

A

Disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain

310
Q

What are the causes of cerebral palsy?

A
  1. Antenatal (80%): e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV)
  2. Intrapartum (10%): birth asphyxia/trauma
  3. Postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma
311
Q

What are the different types of cerebral palsy?

A
  1. Spastic (70%): hemiplegia, diplegia or quadriplegia
  2. Dyskinetic
  3. Ataxic
  4. Mixed
312
Q

What are the clinical features of cerebral palsy?

A
  1. Abnormal tone early infancy
  2. Delayed motor milestones
  3. Abnormal gait
  4. Feeding difficultie.
313
Q

What diseases are associated with cerebral palsy?

A
  1. Learning difficulties (60%)
  2. Epilepsy (30%)
  3. Squints (30%)
  4. Hearing impairment (20%)
314
Q

What is the management for cerebral palsy?

A
  1. MDT appraoch
  2. Spasticity include oral diazepam, oral and intrathecal baclofen, botulinum toxin type A, orthopaedic surgery and selective dorsal rhizotomy
  3. Anticonvulsants, analgesia as required
315
Q

WHAT IS CAUDA EQUINA SYNDROME?

Where is the damage?

A

Compression of nerve roots

Spinal damage distal to L1

316
Q

What vertebrae are involved with cauda equina?

A

L4 and L5

317
Q

What is the treatment for cauda equina?

A
  1. Surgical decompression by full laminectomy
318
Q

What is the difference between cauda equina and sciatica?

A

In cauda equina you get

  1. Saddle anaesthesia
  2. Bladder dysfunction
  3. Sexual dysfunction
  4. Decreased anal tone

Sciatica is just

  1. Back pain
319
Q

What are the symptoms of cauda equina?

A

Foot drop

Numbness

Saddle anesthesia

Bladder and Bowel incontinence

320
Q

What are the tests for cauda equina syndrome?

A
  1. URGENT MRI - Within 6 hours
321
Q

What is a myelopathy and what causes it?

What is the treatment?

A
  1. Myelopathy= CORD gives UMN
  2. Oseophytes
  3. Disc prolapse (slower onset)
  4. Tumour (slow onset)
  5. Surgical decompression
322
Q

What is a radiculopathy and what causes it?

What is the treatment?

A

Radiculopathy

  1. NERVE ROOT gives LMN

Caused by:

  1. Disc prolapse
  2. Osetoarthrits

Treatment:

  1. Conservative
323
Q

WHAT IS SCIATICA?

A

Pain in the distribution of the sciatic nerve, ie felt in the thigh and, MOST IMPORTANTLY, below the knee

A pain that is not felt below the knee is not sciatica

324
Q

What is the treatment for sciatica?

A
  1. Conservative treatment for 6-8 weeks.
    Keep active
    Provide - paracetamol, NSAIDs, codiene, morphine
  2. Steroid injections

If pain doesn’t improve after 6-8 weeks then you should refer to MSK

  1. Surgery
    Laminectomy
    Discetomy
325
Q

What are the investigations for sciatica?

A
  1. MRI
  2. Check for red flags
    e. g. malignancy, fractures, cauda equina syndrome
  3. Pain on straight leg raise
326
Q

What are the cuases of sciatica?

A
  1. Disc herniation:
    Common sites of herniation are L4-L5 and L5-S1
  2. Malignancy
  3. Infection
  4. Vascular compression
327
Q

What are the risk factors for sciatica?

A

Personal factors including:
Age (peak 45-64 years)
Increasing risk with height
Smoking
Psychological stress

Occupational factors include:
Strenuous physical activity - for example, frequent lifting, especially while bending and twisting
Driving
Vibration of the whole body

328
Q

What is the anatomy of the spine?

What happens in cauda equina?

A

Nucelus pulposus surrounded by annulus fibrosis

Herniates out and compresses spine

329
Q

WHAT IS SPINAL STENOSIS?

A

Lumbar spinal stenosis is a condition in which the central canal is narrowed by tumour, disk prolapse or other similar degenerative changes.

330
Q

What are the clinical features of spinal stenosis?

A
  1. Back pain, buttocks, thighs or legs
  2. Cramping of burning feeling
  3. Problems with balance
  4. Sensory loss
  5. Muscle weakness
331
Q

How do you differentiate neurogenic vs vascular claudication?

A
332
Q

What are the investigations for spinal stenosis?

A
  1. MRI
333
Q

What is the treatment for spinal stenosis?

A
  1. Laminectomy
334
Q

WHAT IS A MONONEUROPATHY?

A

Disease of a single peripheral or cranial nerve is called a mononeuropathy. It may be associated with systemic illnesses such as diabetes mellitus, sarcoidosis, rheumatoid arthritis or polyarteritis nodosa. The most common cause worldwide is leprosy.

335
Q

What are the causes of median nerve palsy?

A
  1. Humerus fracture
  2. Carpal tunnel syndrome
336
Q

What are the clinical features of median nerve palsy?

A
  1. Paralysis of thenar muscles, oppenens pollicis
  2. Loss of sensation in the palmar aspect of lateral 3 1/2 fingers
337
Q

What is seen on an EMG for carpal tunnel syndrome?

A

Motor + sensory: prolongation of the action potential

338
Q

What is the treatment for carpal tunnel syndrome?

A
  1. Corticosteroid injection
  2. Wrist splints at night
  3. Surgical decompression (flexor retinaculum division)
339
Q

WHAT ARE THE CAUSES OF RADIAL NERVE PALSY?

A
  1. Crutch palsy’ - due to compression of the nerve above the spiral groove by crutches as the weight is borne in the axilla
  2. Saturday night palsy’ - due to compression of the nerve in the upper part of the arm as a result of resting the medial side of the arm against a sharp edge such as the back of a chair for a prolonged period. The person is usually intoxicated. It may also be seen after surgery when the anaesthetised patient is allowed to hang over the edge of the operating theatre table.
  3. Humeral fracture of the shaft
  4. Rarely, dislocation of the elbow
340
Q

What are the clinical features of radial nerve palsy?

A
  1. Weakness of forearm extension and flexion - triceps and brachioradialis
  2. Wrist drop and finger drop - paralysis of the extensors of the wrist and digits
  3. Weakness of the long thumb abductor and extensor muscles
  4. Sensory loss on the dorsum of hand and forearm appropriate to the cutaneous distribution - see radial nerve anatomy
341
Q

What is the treatment for radial nerve palsy?

A
  1. Splint in extensor position
  2. Should heal within 4 to 8 months
342
Q

WHAT ARE THE CAUSES OF A ULNAR NERVE PALSY?

A
  1. Elbow behind the medial epicondyle
343
Q

What are the clinical features of ulnar nerve palsy?

A
  1. Wasting and weakness of the small muscles of the hand and partial clawing of the ring and little finger
  2. Hypothenar eminence
  3. Weakness of thumb adduction and abduction
  4. Loss of sensation of the little and ring finger
344
Q

What is the treatment for ulnar nerve palsy?

A
  1. Avoidance of full elbow flexion
  2. Decompression of nerve
345
Q

WHAT ARE THE CAUSES OF AXILLARY NERVE LESION?

A
  1. Dislocation of shoulder
  2. Break of humerus
346
Q

What are the clinical features of axillary nerve lesion?

A
  1. Loss of sensation over a small area of skin on the lateral aspect of upper arm
  2. Loss of function of the deltoid muscle, inability to initate abduction of the arm from a position of zero abduction.
347
Q

What is the treatment for axillary nerve palsy?

A
  1. Splinting in a position of abduction at the shoulder
348
Q

WHAT ARE THE CAUSES OF PERONEAL NERVE PALSY?

A
  1. Acute trauma - direct blows and laceration
  2. External pressure - Nerve compression, sitting cross-legged
349
Q

What are the clinical features of common peroneal nerve palsy?

A
  1. Foot drop
  2. Weakness of dorsiflexion of the foot
350
Q

What is the treatment for common peroneal nerve palsy?

A
  1. Should self resolve if a result of compression
351
Q

WHAT ARE THE CAUSES OF LONG THORACIC NERVE PALSY?

A
  1. Often occurs during sport after a blow to the ribs
  2. Mastectomy
352
Q

What are the clinical features of long thoracic nerve lesion?

A
  1. Winging of the scapula
353
Q

What is the treatment for long thoracic nerve palsy?

A
  1. Usually nothing, self resolving
354
Q

WHAT IS SPINAL CORD COMPRESSION?

A

Spinal cord compression is characterised by a combination of a progressive history of neurological deficit and a sensory level on examination.

355
Q

What are some caues of spinal cord compression?

A
  1. Trauma
  2. Congenital bone anomalies
  3. Disc prolapse
  4. Neoplasia
  5. Abscess
356
Q

What are the clinical features of spinal cord compression?

A

Depends on:

  1. Site of lesion - intramedullary lesions produce within spinal segmental damage only; others produce cord both root and segmental damage
  2. Extent of lesion - partial, e.g. Brown Sequard, or complete
  3. Level of lesion - roots only damaged below L1
  4. Speed of onset - rapidly progressive lesions usually produce permanent deficits
  5. ‘Spinal shock’ - upper motor neurone disease - but with a flaccid paralysis, loss of reflexes, absent plantar reflexes
357
Q

What are the investigations for spinal cord compression?

A
  1. FBC, U&E, kidney function, LFTs
  2. Chest x-ray
  3. Spinal x-ray
  4. MRI - investigation of choice
358
Q

What is the treatment for spinal cord compression?

A
  1. Analgesia
  2. Bispohphonates
  3. Radiotherapy
  4. Vertebroplasty
  5. Corticosteroids - particularly in neoplastic spinal cord compression
359
Q

WHAT IS A SUBARACHNOID HAEMORRHAGE?

A

—Rupture of the arteries forming the circle of Willis

—Often because of ‘Berry aneurysms’

360
Q

What are the causes of subarachnoid haemorrhages?

A
  1. Trauma
  2. Berry aneurysm
  3. Arteriovenous (AV) malformations
  4. Idiopathic
361
Q

What are the signs and symptoms of a subarchanoid haemorrhage?

What is the headache called which they call a warning sign of a leaky vessel?

A

Symptoms

  1. —Sudden onset severe headache (—‘Thunderclap headache’)
  2. Meningism
  3. Photophobia
  4. Reduced consciousness
  5. Vomiting
  6. Collapse

Sign

  1. Kernig’s sign
  2. Terson syndrome (retinal, subhyaloid and vitreous bleeds)
  3. 3rd oculomotor palsy (posterior communicating artery)
  4. Sentinel headache
362
Q

What are the investigations for a subarchanoid haemorrhage?

A
  1. CT
    • Spider sign
  2. LP
    • CSF bloody early
    • Becomes xanthochromic (yellow), breakdown of haem to bilibrubin
    • Normal or raised opening pressure
  3. Angio
    • To determine location
363
Q

What is the treatment for subarchanoid haemorrhage?

A
  1. Neurosurgery!!!!
  2. Nimodipine (recued vasospasm)
  3. If anneurysm deteced either coil or clipping
364
Q

What complication occurs following subarachnoid haemorrhage?

Therefore what blood test should be done?

A
  1. Hyponatraemia
  2. Urea and electrolytes
365
Q

WHAT ARE THE CAUSES OF RAISED ICP?

A
  1. Idiopathic intracranial hypertension
  2. Traumatic head injuries
  3. Infection
    • meningitis
  4. Tumours
  5. Hydrocephalus
366
Q

What are the features of raised ICP?

A
  1. Headache
  2. Vomiting
  3. Reduced levels of consciousness
  4. Papilloedema
  5. Cushing’s triad
    • Widening pulse pressure
    • Bradycardia
    • Irregular breathing
367
Q

what investigations and monitoring is there for raised ICP?

A
  1. Neuroimaging (CT/MRI)
    • ​​Effacement of the cerebral ventricles and loss of grey-white matter differentiation
  2. Invasive ICP monitoring
    • Catheter placed into the lateral ventricles of the brain to monitor the pressure
    • May also be used to take collect CSF samples and also to drain small amounts of CSF to reduce the pressure
    • A cut-off of > 20 mmHg is often used to determine if further treatment is needed to reduce the ICP
368
Q

What is the management of raised ICP?

A
  1. Investigate and treat the underlying cause
  2. head elevation to 30º
  3. IV mannitol may be used as an osmotic diuretic
  4. Controlled hyperventilation
    • aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
    • leads to rapid, temporary lowering of ICP. However, caution needed as may reduce blood flow to already ischaemic parts of the brain
  5. Removal of CSF, different techniques include:
    • drain from intraventricular monitor (see above)
    • repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
    • ventriculoperitoneal shunt (for hydrocephalus)
369
Q

WHAT ARE SOME CAUSES OF COMA?

A
  1. Drug overdose
  2. Metabolic causes
  3. Acute central nervous system infection
  4. Acute systemic infection
  5. Cerebral vascular causes
  6. Cerebral pressure causes
  7. A variety of other causes, of which the principal is head injury
370
Q

What is the definition is brainstem death?

A

Brainstem death is the point at which the brain has ceased to be capable of maintaining life. It is a concept which has developed from the advent of improved intensive care facilities and better resuscitation techniques.

371
Q

What are the stages of certifying brainstem death?

A
  1. Ensure certain pre-conditions - relating to the patient and to the staff involved
  2. Perform the diagnostic tests - two sets, usually within 24 hours depending upon the primary pathology and the course of the disease
  3. Record results - by hand and in the notes to avoid possible tampering
372
Q

What is cortical brain death?

A

In cortical brain death, the cortex is destroyed. Often the brainstem is still intact, e.g. persistent vegative state, i.e. the patient can survive indefinitely if sufficient nutrition

373
Q

How do you diagnose cortical brain death?

A

For this condition to be diagnosed there must be a demonstration of no perfusion of the cortex via cerebral angiography. It is not sufficient to just show no EEG activity.

374
Q

WHAT IS A BRAIN ABSCESS?

A

Brain abscess is a focal collection of pus within the brain parenchyma. Abscesses can develop as a result of:

375
Q

What are the causes of brain abscesses?

A
  1. Haematogenous spread
    • Usually, from a primary site in the heart, lung or distal bones - for example:
      • Subacute bacterial endocarditis - usually causing multiple abscesses
  2. Direct implantation of organisms
    • Usually, trauma, neurosurgery
  3. Local extension from adjacent foci
    • Suppurative otitis media } mainly to temporal lobe
  4. Mastoiditis } less to cerebellum
  5. Impaired immunity / diabetes
376
Q

What are the symptoms of a brain abscess?

A
  1. Headache - dull
  2. Fever
  3. Focal neurology - oculomotor nerve palsy or abducens nerve palsy
377
Q

What are the investigations for a brain abscess?

A
  1. CT
378
Q

What is the treatment for a brain abscess?

A
  1. Surgery
    • A craniotomy is performed and the abscess cavity debrided
    • The abscess may reform because the head is closed following abscess drainage.
  2. IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
  3. Intracranial pressure management: e.g. dexamethasone
379
Q

WHAT ARE MYOPATHIES?

A

Myopathies are diseases of muscle.

Like neuropathies, myopathies are characterised by:

  1. Muscle weakness
  2. Muscle atrophy​
  3. The pattern of muscle weakness seen in myopathies is usually proximal and symmetrical - this compares with a distal, or nerve or root distribution seen in neuropathies.
  4. Tone normal or reduced
  5. Reflexes normal or reduced

Sensory loss is not seen in myopathies.

380
Q

What is steroid myopathy?

What is the treatment?

A
  1. Proximal muscle weakness
    Also contibute by hypokalaemia
  2. Minimise corticosteroid excess
381
Q

WHAT IS MYOTONIC DYSTROPHY?

A

Inherited myopathy with features developing at around 20-30 years old.

It affects skeletal, cardiac and smooth muscle

382
Q

What is the cause of myotonic dytrophy?

A

Autosomal dominant

383
Q

What are the clinical features of myotonic dystrophy?

A
  1. Myotonic facies (long, ‘haggard’ appearance)
  2. Frontal balding
  3. Bilateral ptosis
  4. Cataracts
  5. Dysarthria
384
Q

What are the complications of myotonic dystrophy?

A
  1. Cardiac arrhythmias
  2. Abnormalities of glucose/insulin metabolism
  3. Reproductive dysfunction
385
Q

What are the investigations for myotonic dystrophy?

A
  1. Slightly raised CPK enzyme levels
  2. Conduction abnormalities on ECG
  3. Characteristic myopathic EMG, with so-called dive bomber noise
  4. Cataracts may be seen by slit lamp examination
  5. If urinary glucose is positive, it is followed by glucose tolerance test to confirm diabetes
386
Q

What is the treatment for myotonic dystrophy?

A
  1. Membrane stabilisers to reduce myotonia, including procainamide, phenytoin, quinine, quinidine, acetazolamide
  2. Identification and treatment of cataracts and diabetes mellitus
  3. Genetic counselling
  4. Avoiding sedative drugs as sensitivity is increased
387
Q

WHAT ARE THE SYMPTOMS OF STATIN MYOPATHY?

A
  1. Myalgia
  2. Myositis
  3. Rhabdomyolysis
  4. Asymptomatic raised creatine kinase
388
Q

WHAT IS DUCHENNE MUSCULAR DYSTROPHY?

A

Duchenne muscular dystrophy is a common and possibly the best known muscular dystrophy. It follows an aggressive and progressive course.

389
Q

What is the inheritance of duchenne muscular dystrophy?

A

X-linked

390
Q

What are the clinical features of duchenne muscular dystrophy?

A
  1. Progressive proximal muscle weakness from 5 years
  2. Calf pseudohypertrophy
  3. Gower’s sign: child uses arms to stand up from a squatted position
  4. Associated with dilated cardiomyopathy
  5. 30% of patients have intellectual impairment
391
Q

What are the investigations for duchenne muscular dystrophy?

A
  1. CK 30 to 200 times higher than normal
392
Q

What is the management of Duchenne muscular dystrophy?

A

Largely supportive

  1. Mobility aids
  2. Steroids
  3. ACEI
393
Q

WHAT ARE THE UPPER MOTOR SIGNS?

A
  1. Weakness - the extensors are weaker than the flexors in the arms, but the reverse is true in the legs
  2. Muscle wasting is absent or slight - muscle wasting is prominent in a lower motor neurone lesion
  3. Hyper-reflexia and clonus - reflexes are absent or reduced in a lower motor neurone lesion
  4. Spasticity
  5. No fasciculations - fasciculations occur in a lower motor neurone lesion
  6. Extensor plantar responses
394
Q

WHAT ARE THE LOWER MOTOR SIGNS?

A
  1. Weakness of the muscles innervated
  2. Prominent muscle wasting - slight or absent in upper motor neurone disease
  3. Absent or reduced reflexes - there are increased reflexes in upper motor neurone disease
  4. Hypotonicity
  5. Fasciculations - absent in upper motor neurone disease
  6. Flexor or absent plantar responses
395
Q

What does the trigeminal nerve do?

What are the branches called?

A

Sensation to the face

Three branches

  1. Opthalmic
  2. Maxillary
  3. Mandibular
396
Q

WHAT IS AN ESSENTIAL TREMOR?

A

Essential tremor (previously called benign essential tremor) is an autosomal dominant condition which usually affects both upper limbs

397
Q

What are the features of an essential tremor?

A
  1. postural tremor: worse if arms outstretched
  2. improved by alcohol and rest
  3. most common cause of titubation (head tremor)
398
Q

What is the management of an essential tremor?

A
  1. propranolol is first-line
  2. primidone is sometimes used
399
Q

WHICH DERMATOME INNERVATES THE THUMB AND INDEX FINGER?

A

C6

400
Q

Which dermatome innervates the middle finger and palm?

A

C7

401
Q

What is Erb-Duchenne paralysis?

A
  1. Damage to C5,6 roots
  2. Winged scapula
  3. May be caused by a breech presentation
402
Q

What is Klumpke’s paralysis?

A
  1. Damage to T1
  2. Loss of intrinsic hand muscles
  3. Due to traction
403
Q

HOW CAN YOU QUICKLY CHECK THE FLUID DRIPPING FROM BACK OF THE NOSE TO SEE IF IT IS CSF?

A
  1. Beta-2 transferrin
  2. If not available glucose
404
Q

ABOVE WHAT LEVEL DOES AUTONOMIC DYSREFLEXIA OCCUR?

What is it triggered by?

A

T6

Faecal impaction or urinary retention

405
Q

WHAT IS THE TREATMENT FOR LOW PRESSURE HYDROCEPHALUS?

A
  1. Caffeine
  2. Fluids
406
Q

When does low pressure hydrocephalus oocur?

A

After a lumbar puncture

407
Q

WHAT ARE THE FEATURES OF RESTLESS LEG SYNDROME?

A
  1. uncontrollable urge to move legs (akathisia). Symptoms initially occur at night but as condition progresses may occur during the day. Symptoms are worse at rest
  2. paraesthesias e.g. ‘crawling’ or ‘throbbing’ sensations
  3. movements during sleep may be noted by the partner - periodic limb movements of sleeps (PLMS)
408
Q

What are the associations with restless leg syndrome?

A
  1. there is a positive family history in 50% of patients with idiopathic RLS
  2. iron deficiency anaemia
  3. uraemia
  4. diabetes mellitus
  5. pregnancy
409
Q

What is the management of restless leg syndrome?

A
  1. simple measures: walking, stretching, massaging affected limbs
  2. treat any iron deficiency
  3. dopamine agonists are first-line treatment (e.g. Pramipexole, ropinirole)
  4. benzodiazepines
  5. gabapentin
410
Q

WHAT IS CREUTZFELDT-JAKOB DISEASE?

A

Creutzfeldt-Jakob disease (CJD) is rapidly progressive neurological condition caused by prion proteins. These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.

411
Q

What are the features of Creutzfeldt-Jakob disease?

A
  1. Dementia (rapid onset)
  2. Myoclonus
412
Q

What are the investigations for Creutzfeldt-Jakob disease?

A
  1. CSF is usually normal
  2. EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
  3. MRI: hyperintense signals in the basal ganglia and thalamus
413
Q

WHAT IS CHARCOT-MARIE-TOOTH?

A

Charcot-Marie-Tooth disease is a hereditary sensory and motor peripheral neuropathy. UMN signs are not present in these patients. Patients can present with lower motor neurone signs in all limbs and reduced sensation (more pronounced distally).

414
Q

WHAT DOES A BASILAR ARTERY STROKE CAUSE?

A

‘Locked-in’ syndrome

415
Q

WHAT IS SUBACUTE COMBINED DEGENERATION OF SPINAL CORD?

A
  1. due to vitamin B12 deficiency
  2. dorsal columns + lateral corticospinal tracts are affected
  3. joint position and vibration sense lost first then distal paraesthesia
  4. upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
  5. if untreated stiffness and weakness persist
416
Q

What are the indications for urgent CT scan?

A
  1. GCS < 13 on initial assessment
  2. GCS < 15 at 2 hours post-injury
  3. suspected open or depressed skull fracture.
  4. any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
  5. post-traumatic seizure.
  6. focal neurological deficit.
  7. more than 1 episode of vomiting
417
Q

What are the indications for a CT scan within 8 hours?

A
  1. age 65 years or older
  2. any history of bleeding or clotting disorders
  3. dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs)
  4. more than 30 minutes’ retrograde amnesia of events immediately before the head injury
  5. If a patient is on warfarin who have sustained a head injury with no other indications for a CT head scan, perform a CT head scan within 8 hours of the injury.

ΩΩ 3a Bateman - Neuro + Cardio (2 decks)

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