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Sirpi's Phase 2A Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the function of the corticospinal tract?

A

Voluntary movement control.

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2
Q

What is the path of the corticospinal tract?

A

Originates at the primary motor cortex in the frontal lobe.

Lateral corticospinal tract decussates at the medullary pyramids.

Anterior corticospinal tract continues ipsilaterally and synapses at the ventral grey horn at the spinal cord where it decussates.

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3
Q

What would be a result of a spinal cord lesion in the corticospinal tract?

A

Ipsilateral loss of movement (paralysis) due to decussation mainly occuring in the medullary pyramids.

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4
Q

What is the function of the DCML tract?

A

Fine touch, proprioception, sensation, vibration, 2 point discrimination.

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5
Q

What is the pathway of the DCML tract?

A

1st = sensory neuron ascends ipsilateraly through dorsal columns.

Synapses at gracile (LL) or cuneate (UL) fasciculus.

Decussates at the medulla before reaching tertiary neuron in thalamus then primary somatosensory cortex.

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6
Q

What would be a result of a spinal cord lesion in the DCML tract?

A

Ipsilateral loss of fine touch, proprioception, sensation, vibration and 2 point discrimination,

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7
Q

What is the function of the spinothalamic tract?

A

Pain, temperature sensation.

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8
Q

What is the pathway of the spinothalamic tract

A

Primary sensory neuron from nociceptors synapses with secondary neuron in ventral grey horn.

Decussates a few levels above entry point into spinal cord.

Ascends ipsilaterally into tertiary neuron in thalamus.

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9
Q

What would be a result of a spinal cord lesion in the spinothalamic tract?

A

Contralateral loss of pain and temperature sensation.

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10
Q

What is an Extradural Haemhorrage?

A

Haemorrhage between dura mater and skull.

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11
Q

Aetiology of Extradural Haemorrhage

A

Traumatic injury

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12
Q

What is the Source and Nature of Bleeding in an Extradural Haemorrhage

A

Injury such as skull fracture can cause rapid bleeding of meningeal arteries.

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13
Q

Clinical Presentation of Extradural Haemorrhage

A

Patient may be initially ok
Gradual neurological deterioration e.g onset of headache, drowsiness, confusion.
Due to rapid rise in intracranial pressure

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14
Q

Investigation of Extradural Haemorrhage

A

CT head
Acute bleed appears hyperdense (bright white) on CT.
Convex, lemon-like appearance that is concentrated in an area due to dural attachments limiting the spread of blood.
Can result in midline shift

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15
Q

What is midline shift?

A

Compression of the brain causing falx cerebri being pushed away from middle.

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16
Q

What is a Subdural Haemorrhage?

A

Haemorrhage between the dura and the arachnoid mater.

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17
Q

Aetiology of Subdural Haemorrhage

A

Trauma

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18
Q

What is the Source and Nature of Bleeding in a Subdural Haemorrhage?

A

Results in bleeding of dural bridging veins.
Can cause low pressure and slower bleed due to venous blood.
Slower bleed = slower rise in ICP

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19
Q

Clinical Presentation of Subdural Haemhorrage

A

Onset of symptoms may be days/weeks after injury.
Fluctuating levels of consciousness.

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20
Q

Investigation of Subdural Haemorrhage

A

FL: CT head
Chronic (old) bleed appears hypodense (dark) on CT
Concave (crescent-like) appearance that follows the contours of the brain as it is not limited by dural attachments.
Can have midline shift.

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21
Q

What is a Subarachnoid Haemorrhage?

A

Haemorrhage into the subarachnoid space between the arachnoid and pia mater.

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22
Q

Aetiology of Subarachnoid Haemorrhage

A

Trauma
Aneurysmal rupture e.g berry aneurysm
Arteriovenous malformation

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23
Q

What is the Source and Nature of Bleeding in a Subarachnoid Haemorrhage?

A

Rapid bleeding of cerebral arteries

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24
Q

Clinical Presentation of Subarachnoid Haemorrhage

A

Sudden onset, severe “thunderclap” headache.
Neck stiffness.

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25
Q

Differential Diagnosis for Subarachnoid Hemorrhage

A

Migraine headache
Meningitis
Ischaemic stroke

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26
Q

Investigation of Subarachnoid Haemorrhage

A

CT head
Acute, hyperdense (white) blood.
Blood is seen in fissures and cisterns giving starfish-like appearance.

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27
Q

Complications of Subarachnoid Haemorrhage

A

Blood in SA space can irritate the meninges.
Irritate the cerebral vessels and can cause vasospasm and hypoxic injury.
Can track back into the ventricular system to cause hydrocephalus.

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28
Q

What is an Intracerebral Haemorrhage?

A

Haemorrhage within the brain parenchyma.

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29
Q

Aetiology of Intracerebral Hemorrhages

A

Aneurysm rupture
Amyloidosis
Arteriovenous malformation
Hypertension

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30
Q

Investigation of Intracerebral Haemorrhage

A

Acute, hyperdense (white) bleeding.
Blood seen in the parenchyma of the brain.
Can cause mass effects e.g midline shift if large enough.

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31
Q

What is Meningitis?

A

Inflammation of the meninges

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32
Q

Non-Organismal Aetiology of Meningitis

A

SLE
Vasculitis

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33
Q

Viral Aetiology of Meninigitis

A

Herpes simplex virus
Varicella zoster virus
Epstein-Barr virus

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34
Q

Bacterial aetiology of acute meningitis (regardless of age group)

A

SHENGL

S.pneumoniae
H.influenzae B
E.coli
N.meningitidis
Group B strep
Listeria monocytogenes - immunocompromised such as newborn, old age, pregnant.

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35
Q

Bacterial aetiology of chronic meningitis

A

M.tuberculosis
Cryptocococcus neoformans fungi
T.pallidum (syphilis)

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36
Q

Bacterial aetiology of meningitis in newborns

A

GEL

Group B strep - can be present in maternal genital tract.
E.coli
L.monocytogenes - IV amoxicillin

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37
Q

Bacterial aetiology of meningitis in ages of children (6months-6 years)

A

NHS

N.meningitidis
H.influenzae B
S.pneumoniae

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38
Q

Bacterial aetiology of meningitis in 6-60 years

A

SN

S.pneumoniae (rarely)
N.meningitidis

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39
Q

Bacterial aetiology of meningitis in those above 60

A

SHNGLE

S pneumoniae
H influenzae type b
N meningitidis
Group B Streptococcus
Listeria monocytogenes

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40
Q

Risk Factors for Meninigitis

A

Immunocompromise
Pregnancy
Old age
Infancy

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41
Q

Pathophysiology of Meningitis

A

Aerosol spread.
Colonises upper RT
Can get into the bloodstream to infect the meninges.

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42
Q

Clinical Presentation of Meningitis

A

Photophobia
Headache
Stiff neck

Non blanching purpuric rash - N.meningitidis

TB Meninigitis
Fever
Night sweats

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43
Q

Examination of Meningitis

A

Kernig’s sign - extension of knee while hip is flexed causes pain.

Brudzinski’s sign - flexion of neck causes reflex flexion of hip and knee.

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44
Q

What is the causative organism of a non-blanching purpuric rash in meningitis?

A

N.meningitidis

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45
Q

Differential Diagnoses of Meningitis

A

Subarachnoid haemhorrage
Sinusitis
Malaria
Brain abscess

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46
Q

Investigation of Meningitis

A

FBC: leukocytosis
Raised ESR/CRP

GS: Lumbar puncture with CSF culture.

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47
Q

What features of the CSF are noted in lumbar puncture when checking for meningitis?

A

Appearance
Presence of cells
Protein levels
Glucose levels

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48
Q

What would be the differnce in CSF appearance of viral vs bacterial vs TB/cryptococal meningitis?

A

Viral = clear T

B/cryptococcal = fibrin web appearance

Bacterial = cloudy

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49
Q

What cells would be present in the CSF in viral vs bacterial vs TB/cryptococal meningitis?

A

Viral & cryptococcal = lymphocytes

Bacterial = neutrophils

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50
Q

What would be levels of protein present in the CSF in viral vs bacterial vs TB/cryptococal meningitis?

A

High protein in all.

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51
Q

What would be levels of glucose present in the CSF in viral vs bacterial vs TB/cryptococal meningitis?

A

Bacterial and TB/cryptococcal = low

Viral = high

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52
Q

Management of Bacterial Meningitis

A

Empirically: IV cefotaxime/ceftriaxone + IV dexamethasone for swelling

For returning travellers: IV vancomycin to cover drug-resistant strep.

Meningitis is a notifiable disease so call Public Health England.

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53
Q

Managment of Meningococcal Meningitis

A

IM benzylpenicillin

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54
Q

What is Encephalitis?

A

Inflammation of the cerebral cortex

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55
Q

Aetiology of Encephalitis

A

Mainly viral

Herpes simplex
Varicella zoster
HIV
Parvovirus.

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56
Q

Clinical Presentation of Encephalitis

A

Fever
Headache
Lethargy
Confusion

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57
Q

Investigations of Encephalitis

A

Brain MRI

Lumbar puncture + culture, PCR for suspected virus.

Blood serology - raised IgG antibodies against causative viruses.

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58
Q

Management of Encephalitis

A

Empirically: IV acyclovir for HSV/RSV.

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59
Q

What is a Transient Ischaemic Attack?

A

Brief, self-limiting episode of neurological dysfunction caused by cerebral ischaemia without infarction.

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60
Q

Clinical Presentation of Transient Ischaemic Attacks

A

Short-lasting, self-resolving symptoms of stroke.

Specific to TIA: Amaurosis fugax - sudden loss of vision in one eye due to embolus passing through retinal artery.

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61
Q

Wht is used to calculate the risk of stroke after a TIA?

A

ABCD2 score

Age > 60yrs = 1
Blood pressure > 140/90mmHg = 1
Clinical features:
Unilateral weakness = 2
Speech disturbance without weakness = 1
Duration of symptoms:
Symptoms lasting >1hr = 2
Symptoms lasting 10-59mins = 1
Symptoms <10 mins = 0
Diabetes = 1

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62
Q

Initial management of TIA

A

300 mg loading dose aspirin

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63
Q

Secondary prevention of TIA

A

Antiplatelet therapy e.g clopidogrel + statin e.g atorvastatin

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64
Q

Types of Strokes

A

Ischaemic Stroke (80%)

Haemhorragic Stroke (20%)

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65
Q

Aetiology of Ischaemic Stroke

A

Large vessel disease (50%)
Small vessel disease (25%)
Cardioembolic (20%)
Rare causes e.g venous thrombosis, aortic dissection (5%)

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66
Q

Aetiology of Haemorrhagic Stroke

A

Primary intracerebral haemorrhage

Subarachnoid haemorrhage

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67
Q

What is an Ischaemic Stroke?

A

An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction.

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68
Q

Pathophysiology of Small Vessel Ischaemic Stroke

A

Small deep perforator arteries blocked due to microatheroma/lipohyalinosis.

Caused by high blood pressure, diabetes, smoking, age

Can also be known as lacunar stroke.

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69
Q

Pathophysiology of Cardioembolic Stroke

A

Embolus from the heart becoming a thrombus in brain vessels.

Can be caused by AF, endocarditis, atrial septal defect.

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70
Q

What is a common cause of stroke in younger patients (<45 years)

A

Stroke due to aortic dissection

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71
Q

What is the difference between subarachnoid/intracerebral haemorrhages and subarachnoid/intracerebral haemorrhagic stroke?

A

Haemhorragic strokes are not caused by trauma.

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72
Q

Risk Factors for Stroke

A

Increasing age
Smoking
Arrhythmias e.g atrial fibrillation
Infective endocarditis
Obesity
Hypertension
Vasculitis
Ischaemic heart disease

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73
Q

What is the initial assessment test used to recognize stroke?

A

FAST

Facial drooping
Arm weakness
Speech difficulties
Time

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74
Q

Clinical Presentation of ACA Stroke

A

Contralateral lower limb paralysis and sensory loss.

Urinary incontinence

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75
Q

Clinical Presentation of MCA Stroke

A

Contralateral facial and upper limb paralysis and sensory loss.
Facial drooping

Dominant Hemisphere (usually left):
If in dominant hemisphere, can cause Broca’s aphasia.
Dyslexia
Dysgraphia (writing difficulty)

Non-Dominant Hemisphere (Usually right):
Anosognosia - neglect (unawareness) of paralysed limb

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76
Q

Clinical Presentation of PCA Stroke

A

Contralateral homonymous hemianopia
Unilateral headache

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77
Q

Clinical Presentation of Cerebellar Artery Stroke

A

Nausea/vomiting
Vertigo
Unsteadiness
Ataxia

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78
Q

Differential Diagnoses for Strokes

A

Epileptic seizure
Multiple sclerosis
Migraine
Subdural haemorrhage

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79
Q

Investigation of Stroke

A

First line: CT head - can rule out things like haemorrhage and tumours.

Gold standard: MRI brain with diffusion weighted imaging

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80
Q

Conservative Management of Ischaemic/Haemhorragic Stroke

A

Monitor oxygen, blood pressure, glucose and hydration.

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81
Q

Management of Ischaemic Stroke

A

Thrombolysis if within 4.5 hours post symptom onset.

Administer IV alteplase (tissue plasminogen activator)

Thrombectomy - interventional removal of the thrombus

If presenting after 4.5 hours of symptoms/thrombolysis is contraindicated.

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82
Q

Management of Haemhorragic Stroke

A

Reverse any anticoagulation.

Neurosurgery.

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83
Q

Secondary Prevention of Stroke

A

Antiplatelets e.g low dose clopidogrel + statin e.g atorvastatin

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84
Q

What are the different types of brain tumours?

A

Gliomas - glial cells
Meningiomas - meninges
Craniopharyngiomas - sellar region
Schwannoma - nerve myelin
Primary CNS lymphoma - haematopoetic

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85
Q

Types of gliomas

A

Astrocytoma - most common

Oligodendrocytoma

Ependymoma

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86
Q

What tumours metastasize to the brain?

A

Lung (non small cell - most common vs small cell)
Breast
Colorectal
Testicular
Renal cell
Malignant melanoma

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87
Q

Grading of Brain Tumours

A

Graded 1-4

Grade 1: Slow growing, non-malignant, and associated with long-term survival

Grade 2: Have cytological atypia. These tumours are slow growing but recur as higher-grade tumours.

Grade 3: Have anaplasia and mitotic activity. These tumours are malignant

Grade 4: Anaplasia, mitotic activity with microvascular proliferation, and/or necrosis. These tumours reproduce rapidly and are very aggressive malignant tumours.

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88
Q

Aetiology/risk factors for Gliomas

A

Ionising radiation
Family history
Immunosuppression (CNS lymphoma)
Vinyl chloride exposure

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89
Q

Clinical Presentation of Brain Tumours

A

Headache - raised ICP
Seizures - more in low grade tumours

Focal neurological symptoms such as VFDs, limb weakness. - more in high grade tumours

Papilloedema (optic disk swelling due to raised ICP causing venous return obstruction)

Cognitive/behaviour issues.

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90
Q

Investigation of Brain Tumours

A

First line: CT head with contrast

Gold standard: MRI head with contrast and brain biopsy

CT CAP for staging.

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91
Q

Management of Gliomas

A

IV dexamethasone to reduce swelling

FL: Surgical resection

SL: Radiotherapy + early chemotherapy e.g temozolomide

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92
Q

Differential Diagnoses for Raised ICP

A

Hydrocephalus

Gliomas e.g astrocytoma

Meningitis

Subarachnoid haemorrhage

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93
Q

What is the Monroe-Kellie Doctrine?

A

Sum of CSF, blood and brain volume is constant.

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94
Q

How does the Monroe-Kellie Doctrine apply to increased CSF pressure?

A

Intracranial space is a compliant system where increased pressure due to tumour will be compensated by CSF drainage into the spine.
However, there comes a point where no more CSF can be relocated, causing raised ICP and symptoms.

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95
Q

Clinical Presentation of Raised ICP

A

Papilloedema
Headache

Cushing’s Triad (response to raised ICP) - bradycardia, irregular respiration and widened pulse pressure (raised systolic, reduced diastolic)

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96
Q

Management of Raised ICP

A

IV mannitol - osmotic diuretic so increased fluid excretion.

Interventional: Lumbar punctures.

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97
Q

Types of Generalized Seizures

A

Tonic-clonic
Myoclonic
Absence
Tonic
Atonic

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98
Q

Clinical Presentation of a Tonic-Clonic Seizure

A

Loss of consciousness

Alternating tonic and clonic phases
Tonic phase - stiffness of limbs
Clonic phase - synchronous jerking of the limbs that slowly becomes less frequent.

Can have incontinence, tongue biting.
Post-ictal confusion, unresponsiveness.

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99
Q

Clinical Presentation of a Myoclonic Seizure

A

No loss of consciousness
Sudden isolated jerk of areas like limbs, trunk.

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100
Q

Clinical Presentation of an Absence Seizure

A

Usually happens in childhood

Ceasing of activity and unresponsiveness for a few seconds.

3 Hz spike and wave activity on EEG.

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101
Q

Clinical Presentation of a Tonic Seizure

A

Sudden increased tone causing stiffness.

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102
Q

Clinical Presentation of an Atonic Seizure

A

Sudden loss of consciousness and muscle tone causing collapse.

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103
Q

What is a Focal Seizure?

A

Starts at a local point in the brain and then spreads towards other regions.

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104
Q

Classification of Focal Seizures

A

Types:
Simple Focal Seizures
Complex Focal Seizures

Location Wise:
Frontal Lobe Seizures
Temporal Love Seizures
Parietal Lobe Seizures
Occipital Lobe Seizures

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105
Q

Clinical Presentation of a Simple Focal Seizure

A

Simple Partial Seizures
Consciousness, memory, awareness intact.

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106
Q

Clinical Presentation of a Complex Focal Seizure

A

Most commonly arise from temporal lobe.
Affects memory/awareness.
Post-ictal confusion.

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107
Q

Clinical Presentation of Frontal Lobe Seizure

A

Can remember series of events
Sporadic movements of upper and lower limbs.
Jacksonian march - seizure progressively goes up/down motor homunculus.

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108
Q

Clinical Presentation of Temporal Lobe Seizure

A

Aura of deja vu, auditory hallucination.

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109
Q

Clinical Presentation of Parietal Lobe Seizure

A

Sensory tingling/numbness

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110
Q

Clinical Presentation of Occipital Lobe Seizures

A

Visual phenomena such as flashing lines, spots.

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111
Q

What is Epilepsy?

A

The recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting in seizures.

Need at least 2 separate seizures to be classified as epilepsy.

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112
Q

What is an Epileptic Seizure?

A

Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain.

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113
Q

Clinical Presentation of an Epileptic Seizure

A

Duration: 30 – 120 seconds
“Positive” ictal symptoms
Negative postictal symptoms.
Stereotypical seizures (in one person, seizures occur in the same way).
May be associated with other brain dysfunction
Typical seizure phenomena: lateral tongue bite, déjà vu etc.

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114
Q

What is Status Epilepticus?

A

Seizures lasting longer than 5 minutes, or 2 or more sezures without reganing consciousness in between.

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115
Q

Management of Status Epilepticus

A

ABC + Supportive therapy

Benzodiazepines (GABA agonist) e.g diazepam, midazolam.

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116
Q

Aetiology of Seizures

A

Head trauma
Brain tumours
Strokes
Dementia
Drugs - SSRIs, lithium

117
Q

Differential Diagnoses for Epilepsy

A

Syncope
Cataplexy
Benign paroxysmal vertigo

118
Q

What is Syncope?

A

Paroxysmal event in which changes in behaviour, sensation and cognitive processes are caused by an insufficient blood or oxygen supply to the brain.

Usually occurs when upright.

119
Q

Clinical Presentation of Syncope

A

Precipitant factors e.g sitting, standing, pain, etc.

Presyncopal symptoms (prodrome) - dizziness, nausea, sweating

Blackout - loss of consciousness, can have jerking or being still.

Recovery - rapid and can have feelings of relief.

120
Q

Types of Syncope

A

Cardiogenic syncope has less warning and in patients with a PMH of heart disease.

Cough syncope - heavy coughing can reduce venous return to heart.

Carotid sinus syncope - pressure on carotid sinus can cause increased vagal tone and reduced BP.

121
Q

What is a Functional Dissociative Seizure

A

Paroxysmal event in which changes in behaviour, sensation and cognitive function caused by mental processes triggered by internal/external aversive stimuli.

122
Q

Clinical Presentation of Functional Dissociative Seizure

A

Duration can be 1-20 minutes

Dramatic asynchronous motor phenomena/thrashing.

Eyes closed

Ictal crying/speaking

Can have PMH of psychiatric illness.

123
Q

Investigation of Seizures

A

Emergency: CT head to check for trauma, tumours

MRI brain

EEG to help support diagnosis if epilepsy.

124
Q

Management of Generalized Epileptic Seizures (excluding absence seizures)

A

FL: Oral sodium valproate - increases activity of GABA, inhibitory neurotransmitter.

SL: Oral carbamazepine/lamotrigine if SV containdicated.

125
Q

Management of Absence Seizures

A

FL: Oral ethosuximide
SL: Sodium valproate/lamotrigine

126
Q

Management of Focal Epileptic Seizures

A

FL: Oral lamotrigine - Na channel antagonist so prevents depolarization.

SL: Oral carbamazepine

127
Q

Surgical Management of Epileptic Seizures

A

Lobectomy

Vagal nerve stimulation

128
Q

Pharmacodynamics of Sodium Valproate

A

Increases activity of GABA, an inhibitory neurotransmitter.

129
Q

Side Effects of Sodium Valproate

A

Hepatitis, tremor, hair loss.

130
Q

Contraindications of Sodium Valproate

A

Teratogenic - contraindicated in women of childbearing age.

131
Q

Pharmacodynamics of Carbamazepine and Lamotrigine

A

Sodium channel blockers - prevents axonal depoarization.

132
Q

Side effects of Lamotrigine

A

Skin rashes, headache, insomnia.

133
Q

Side effects of Carbamezapine

A

Ataxia, aplastic anaemia, diplopia.

134
Q

What are examples of traumatic focal lesions of the brain?

A

Haematoma
Contusions
Lacerations
Infection

135
Q

What are 2 mechanism in which traumatic brain lesions can occur?

A

Contact damage at the source of traumatic impact

Acceleration-deceleration damage.

136
Q

What is a brain contusion?

A

Superficial bruises on the brain

137
Q

What is a brain laceration?

A

A brain contusion significant enough to tear the pia mater.

138
Q

What are examples of traumatic diffuse lesions of the brain?

A

Diffuse axonal injury
Diffuse vascular injury
Cerebral oedema
Hypoxic ischaemia
Herniation

139
Q

What is diffuse axonal injury?

A

Widespread axonal damage

140
Q

Aetiology of diffuse axonal injury

A

Acceleration-deceleration damage.

141
Q

What is diffuse vascular injury of the brain?

A

Multiple petechial haemorrhages throughout the brain.

142
Q

Types of of traumatic cerebral oedema

A

Congestive cerebral oedema
Vasogenic cerebral oedema
Cytotoxic cerebral oedema

143
Q

Pathophysiology of congestive cerebral oedema

A

Vasodilation causes increased cerebral blood volume.

144
Q

Pathophysiology of vasogenic cerebral oedema

A

Leakage of oedema fluid from damaged blood vessels.

145
Q

Pathophysiology of cytotoxic cerebral oedema

A

Passage of extracellular fluid into cells like eurons and glia.

146
Q

Complications of diffuse vascular injury and swelling of the brain?

A

Brain can herniate.

147
Q

Aetiology/risk factors of chronic traumatic encephelopathy

A

Repeated brain traumtic injury.

Football players, boxers
War veterans.

148
Q

Pathophysiology of chronic traumatic encephalopathy

A

Progressive amyloid deposition and TBP-43.

149
Q

Clinical presentation of chronic traumatic encephalopathy

A

Irritability, impulsivity, aggression, memory loss.

Followed by dementia, walking disabilities, parkinsonism.

150
Q

Aetiology/Risk Factors of Parkinson’s Disease

A

Increasing age
Male gender
Family history

151
Q

Pathophysiology of Parkinson’s Disease

A

Progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta.

Presence of lewy bodies.

152
Q

Clinical Presentation of Parkinson’s Disease

A

Triad of bradykinesia, tremor, rigidity.

TRAP

Tremor - pill rolling tremor
Rigidity - cogwheel rigidity
Akinesia/bradykinesia - shuffling gait, assymetrical reduction in arm swing.
Postural impariment - stooped posture

153
Q

Management of Parkinson’s Disease

A

Synthetic Dopamine e.g Levodopa (L-DOPA)

Dopamine Agonists e.g Ropinirole, pramipexole

Monoamine Oxidase (MAO) Inhibitors e.g Rasagiline, Selegiline

154
Q

Aetiology of Huntington’s Disease

A

Autosomal dominant trinucleotide repeat of CAG in the huntingtin (HTT) gene on chromosome 4.

155
Q

Pathophysiology of Huntington’s Disease

A

Trinucleotide repeats have anticipation - earlier onset going down generations.
Atrophy of striatum (caudate and putamen) results in decreased GABA and acetylcholine production.
GABA is inhibitory to dopamine release resulting in excessive thalamic stimulation.

156
Q

Clinical Presentation of Huntington’s Disease

A

ABCD

Abnormal eye movements.
Behavioural changes e.g increased aggression.
Chorea - involuntary jerky movements.
Dysarthria - difficult moving muscles for speech

157
Q

Management of Huntington’s Disease

A

Symptomatic - tetrabenazine/risperidone (dopamine antagonist)

Haloperidol (dopamine receptor antagonist) for psychosis

Can also give diazepam

158
Q

Investigation of Huntington’s Disease

A

Genetic testing for HTT gene mutation.

159
Q

What are the layers of the cerebellum?

A

Molecular Layer
Purkinje cell layer - only output of cerebellar cortex.
Granule cell layer

160
Q

What is Ataxia?

A

Problems with balance and coordination.

161
Q

Inherited Aetiology of Ataxia

A

Autosomal dominant - SCA 6, EA 2 mutations.

Autosomal recessive - Friedreich’s ataxia - most common in UK.

X-linked - Fragile X Tremor Ataxia Syndrome (FXTAS)

Mitochondrial - mDNA mutations

Metabolic - Tay-Sach’s disease

162
Q

Acquired Aetiology of Ataxia

A

Metabolic - alcohol, b12 folate deficiency, drugs e.g lithium.

Immune mediated - paraneoplastic cerebellar degeneration, coeliac.

Infective - post-infectious cerebellitis

Degenerative - multi-system atrophy cerebellar variant (MSA-C) - hot cross bun sign on MRI.

Structural - tumours, vascular causes.

163
Q

Aetiology of Freidrichsen’s Ataxia

A

Trinucleotide repeat in frataxin gene on chromosome 9.

164
Q

Clinical Presentation of Freidrichsen’s Ataxia

A

Cerebellar disease symptoms (DANISH)
High foot arches (pes cavus)
Scoliosis

165
Q

What conditions are Freidrichsen’s Ataxia associated with?

A

Diabetes mellitus
Hypertrophic cardiomyopathy

166
Q

Clinical Presentation of Cerebellar Dysfunction

A

DANISH

Dysdiadochokinaesia - inability to perform rapid, alternating movements.
Ataxia
Nystagmus
Intention tremor
Speech difficulties
Hyper/hypotonicity

167
Q

Staging of Ataxia

A

Mild = Independent mobilisation or needs 1 walking aid

Moderate = Needs 2 walking aids/walking frame

Severe = Wheelchair dependent

168
Q

Investigation of Ataxia

A

Brain MRI

169
Q

Examples of Motor Neuron Disease

A

Amyotrophic lateral sclerosis - mixture of UMN & LMN degeneration

Primary lateral sclerosis - primarily UMN degeneration

Primary muscular atrophy - primarily LMN degeneration

Progressive bulbar palsy - primarily LMN degeneration

170
Q

Pathophysiology of PLS

A

Loss of Betz cells in the motor cortex.

171
Q

Pathophysiology of ALS

A

Familial version can be due to mutation in superoxide dismutase enzyme which causes increased oxidative stress on cells causing loss of function.

172
Q

Common Clinical Presenation of UMND and LMND

A

Oculomotor nerve (eye movements) and Onuf’s nucleus (rectal and urinary sphincters) are spared.
No sensory symptoms

173
Q

Clinical Presentation of Upper Motor Neuron Disease/Lesion

A

Contralateral symptoms to lesion.
Increased tone & spasticity (clasp-knife)
Hyperreflexia
Limb weakness
Positive Babinski reflex
Toes curled up

174
Q

Clinical Presentation of Lower Motor Neuron Disease/Lesion

A

Atrophy, muscle wasting.
Fasciculations - sporadic muscle contractions due to increasing size of motor units causing visible appearance.
Hyporefelxia
Flaccid paralysis of limb.
Negative babinski reflex.
Toes curled down.

175
Q

Clinical Presentation of Progressive Bulbar Palsy

A

Dysarthria
Dysphasia
Jaw spasms

176
Q

Clinical Presentation of Amyotrophic Lateral Sclerosis (ALS)

A

UMND + LMND symptoms

Split hand sign - thumb seems adrift due to Increased thenar (thumb) wasting compared to hypothenar (pinky) wasting.

Wrist & foot drop

177
Q

Clinical Presentation of Primary Lateral Sclerosis (PLS)

A

UMN symptoms with marked leg spasticity.

Progressive tetraparesis (all 4 limb weakness)

178
Q

Clinical Presentation of Primary Muscular Atrophy (PMA)

A

LMN symptoms
Starts at one limb then spreads
Distal muscles affected before proximal muscles.

179
Q

Management of Motor Neuron Disease

A

Riluzole - Na channel blocker and glutamate antagonist

Non-invasive ventilation.

180
Q

What is Dementia?

A

Dementia describes a set of symptoms that may include memory loss and difficulties with thinking, problem-solving or language.

181
Q

Types of Dementia

A

Alzheimer’s Disease - most common
Frontotemporal dementia
Lewy Body dementia
Vascular dementia

182
Q

Risk Factors for Alzheimer’s Disease

A

Increasing age
Down’s syndrome
Associated with ApoE proteins.

183
Q

Pathophysiology of Alzheimer’s Disease

A

Widespread cortical atrophy
Progressive amyloidosis
Formation of neurofibrillary tangles from tau proteins.
Results in Ach deficiency.

184
Q

Clinical Presentation of Alzheimer’s Disease

A

Episodic memory loss (day-to-day memory loss)

Agnosia - failure to recognize objects, people, places.

Language speaking and understanding difficulties.

Apraxia - cannot carry out skilled motor tasks.

185
Q

Investigation of Alzheimer’s Disease

A

Brain MRI - cerebral atrophy

186
Q

Management of Alzheimer’s Disease

A

Acetylcholinesterase inhibitors such as pyridostigmine.

187
Q

Genetic aetiology of frontotemporal dementia

A

Microtuble associated protein tau (MAPT) mutation on chromosome 17.

188
Q

Pathophysiology of Frontotemporal Dementia

A

Frontotemporal lobe degeneration and atrophy.

189
Q

What are the 2 Variants of Frontotemporal Dementia? .

A

Behavioural and Language Variants

190
Q

Clinical Presentation of Language Variant Frontotemporal Dementia

A

Classifications include:
Semantic Dementia
Primary Non-Fluent Aphasia

Presents with progressive aphasia.

191
Q

Clinical Presentation of Behavioural Variant Frontotemporal Dementia

A

Can present with behavioural changes e.g apathy

192
Q

Pathophysiology of Vascular Dementia

A

Results from chronic ischaemia and multiple infarcts.

193
Q

Clinical Presentation of Vascular Dementia

A

Step-wise cognitive decline

Late onset memory impairment.
Apraxic gait
Urinary incontinence

194
Q

Investigation of Vascular Dementia

A

Brain MRI: Widespread small vessel disease.

195
Q

Aetiology/Risk Factors for Lewy-Body Dementia

A

Secondary to Parkinson’s disease

196
Q

Pathophysiology of Lewy-Body Dementia

A

Presence of alpha synuclein deposits (lewy bodies) on cortex.

197
Q

Clinical Presentation of Lewy-Body Dementia

A

Hallucinations
Parkinsonism

198
Q

Management of Lewy-Body Dementia

A

Can be treated with AchE inhibitors e.g pyridostigmine

199
Q

Aetiology/Risk Factors of Multiple Sclerosis

A

Female at increased risk since autoimmune.
20-40 age
EBV

200
Q

Pathophysiology of Multiple Sclerosis

A

T-cell mediated autoimmune CNS demyelination.
Targeted towards oligodendocytes.

Demyelinated plaques around the axons result in reduced transmission speed and efficiency.

Regenerated myelin is much less efficient and is temperature affected.

Repeated demyelination can result in axonal scarring (sclerosis).

201
Q

Types of Multiple Sclerosis

A

Relapsing-Remitting MS
Symptoms occur in attacks followed by periods of remission.

Chronic Progressive MS
Can be primary - worsening progressively from disease onset.
Can be secondary - occuring after relapsing-remitting MS.

202
Q

Clinical Presentation of Multiple Sclerosis

A

Charcot’s neurological triad - dysarthria , nystagmus, intention tremor.

Unilateral optic neuritis - acute painful loss of vision in one eye, worse on movement.

Internuclear opthalmoplegia

Brainstem/cerebellar demyelination - diplopia, vertigo, facial weakness, ataxia.

Spinal cord syndromes - paralysis, parasthesia

203
Q

3 Visual Presentations of Multiple Sclerosis

A

Unilateral optic neuritis - painful acute loss of vision.

Internuclear opthalmoplegia - adduction impairment of ipsilateral eye and nystagmus of contralateral eye.

Diplopia

204
Q

What are 2 Phoenomena associated with Multiple Sclerosis?

A

Lhermittes phoenomenon - neck flexion causes shock-like feeling.

Uhthoff’s phoenomenon - symptoms worsen with temperature.

205
Q

Investigation of Multiple Sclerosis

A

GS: MRI brain and spinal cord - disseminated periventricular plaques.

Lumbar puncture - oligoclonal bands, raised IgG and myelin basic protein.

Evoked potentials - conduction delay.

206
Q

Management of Acute Multiple Sclerosis

A

IV methylprednisolone

207
Q

Mangement of Relapsing-Remitting MS

A

Relapsing-remitting (2 or more relapses within 2 years)

DMD e.g IM/SC interferon beta 1A or 1B

Natalizumab - prevents T lymphocytes crossing BBB

208
Q

Management of Progressive MS

A

Biologics e.g ocrelizumab (anti CD20)

209
Q

What are the 3 types of primary headaches?

A

Migraine
Tension
Cluster

210
Q

Aetiology of Secondary Headaches

A

Meningitis

Subarachnoid Haemorrhage - thunderclap

GCA - jaw claudication, visual loss.

Idiopathic Intracranial Hypertension - bomiting

Medication Overuse Headache

Pregnancy - venous sinus headache

Glaucoma - red eyes, if exposed in a dark room for extended periods.

211
Q

Clinical Presentation of Migraine Headache

A

POUND

Photophobia
One-day duration
Unilateral
Nausea
Disabling

Can have preceding aura.
5 instances needed to be diagnosed as migraine.

212
Q

Management of Migraine Headache

A

NSAIDs/paracetamol + triptans (5-hydroxytryptamine agonists) e.g sumatriptan

Regular migraines - propranolol prophylaxis.

Combined contraceptive pill is contraindicated for migraines.

213
Q

Contraindications of Triptans

A

IHD
Hypertension

214
Q

Clinical Presentation of Tension Headache

A

Non pulsating, Bilateral pain

Feeling of tightness around head.

215
Q

Management of Tension Headache

A

Simple analgesia like aspirin, paracetamol.

216
Q

Clinical Presentation of Multiple Sclerosis

A

Charcot’s neurological triad - diplopia, nystagmus, intention tremor.

Unilateral optic neuritis - acute painful loss of vision in one eye, worse on movement.

Internuclear opthalmoplegia

Brainstem/cerebellar demyelination - diplopia, vertigo, facial weakness, ataxia.

Spinal cord syndromes - paralysis, parasthesia

Lhermittes phoenomenon - neck flexion causes shock-like feeling.

Ursoff’s phoenomenon - symptoms worsen with temperature.

217
Q

Clinical Presentation of Cluster Headache

A

Severe or very severe unilateral orbital, supraorbital and/or temporal pain

Lasting 15-180 minutes if untreated

Headache is accompanied by ipsilateral cranial autonomic features e.g lacrimation, ptosis. and/or a sense of restlessness or agitation

Attacks have a frequency from 1 every other day to 8 per day

Not attributed to another disorder

218
Q

Autonomic Features of Cluster Headache

A

Ptosis *eyelid drooping)
Lacrimation & conjunctival injection (teary, bloodshot eyes)
Meiosis (pupil dilation)
Rhinorrhea

219
Q

Management of Cluster Headache

A

Intranasal or subcutaneous triptans e.g sumatriptan
Verapamil prophylaxis.

220
Q

Clinical Presentation of Trigeminal Neuralgia

A

Unilateral shock-like sensation on face.

Can be triggered by movement such as touching face, brushing, etc.

221
Q

Management of Trigeminal Neuralgia

A

FL: Oral Carbamazepine - GABA agonist

222
Q

Which Headaches have a Typically Unilateral Presentation?

A

Migraine
Cluster
Trigeminal Neuralgia
GCA Headache

223
Q

Types of Peripheral Neuropathies

A

Mononeuropathy - lesion affecting a single nerve.
Mononeuropathy multiplex - lesions affecting several individual nerves.
Polyneuropathy - diffuse symmetrical nerve disease.

224
Q

Aetiology of Mononeuropathy

A

Carpal tunnel syndrome
Ulnar nerve lesion
Radial nerve lesion
Common peroneal nerve lesion
Tibial nerve lesion

225
Q

Pathophysiology of Carpal Tunnel Syndrome

A

Compression of median nerve.

226
Q

Clinical Presentation of Carpal Tunnel Syndrome

A

Aching hand pain especially at night
Paresthesia in index and middle finger and partially thumb, ring finger.
Thenar wasting

Symptoms improved when shaking hand.

227
Q

Examination of Carpal Tunnel Syndrome

A

Phalen’s test - wrist flexion for 1 min = pain, parasthesia in areas innervated by median nerve.

Tinel’s test - tapping of transverse carpal ligament = tingling on areas supplied by median nerve.

228
Q

Investigation of Carpal Tunnel Syndrome

A

Conduction electromyography - can see decreased conduction velocity across median nerve through carpal tunel.

229
Q

Management of Carpal Tunnel Syndrome

A

Wrist splint + steroid injections.

Definitive - decompression surgery.

230
Q

Clinical Presentation of Ulnar Nerve Lesion

A

Claw hand - lack of innervation of medial lumbricals
Cannot cross fingers
Hypothenar wasting.

231
Q

Clinical Presentation of Radial Nerve Lesion

A

Wrist/finger drop

232
Q

Clinical Presentation of Common Peroneal Nerve Lesion

A

Foot drop - inability to dorsiflex foot.
Raised foot arches

233
Q

Clinical Presentation of Tibial Nerve Lesion

A

Cannot tiptoe

234
Q

Aetiology of Mononeuropathy Multiplex & Polyneuropathies

A

WARDS CLID

Wegener’s granulomatosis, polyarteritis nodosa
AIDS/Amyloid
Rheumatoid arthritis
Diabetes mellitus
Sarcoidosis

Charcot-Marie Tooth Syndrome
Leprosy
Inflammatory - GBS
Dietary deficiencies/drugs - vitamin B12, folate, vincristine, cisplatin.

235
Q

Examples of Polyneuropathies

A

Diabetic Neuropathy
Guillain Barre syndrome
Charcot-Marie Tooth Disease

236
Q

What is Guillain Barre Syndrome?

A

Acute, inflammatory ascending polyneuropathy that affects the PNS.

237
Q

Risk Factors for GBS

A

Respiratory/GI infection
Post-pregnancy

238
Q

Infectious Aetiology of GBS

A

CMV infection
EBV
Campylobacter jejuni

239
Q

Pathophysiology of GBS

A

Affects Schwann cells.
Pathogen associated molecular mimicry to Schwann cell antigens can cause an autoimmune attack on the Schwann cells causing demyelination.

240
Q

Clinical Presentation of GBS

A

Follows a GI or respiratory tract infection.
Symmetrical ascending muscle weakness.
Arreflexia.
Limb paralysis

241
Q

Investigation of GBS

A

GS: Nerve conduction studies.

Lumbar puncture - CSF has high protein.

242
Q

Management of GBS

A

IV immunoglobulin
Plasma exchange
LMWH heparin e.g enoxaparin for VTE prophylaxis
FVC monitoring - ventilation needed if resp failure.

243
Q

What is Charcot Marie Tooth Syndrome?

A

Group of hereditary motor and sensory neuropathies

244
Q

What is the Genetic Inheritance of Charcot Marie Tooth Syndrome?

A

Typically autosomal dominant

245
Q

Clinical Presentation of Charcot Marie Tooth Syndrome

A

Distal limb wasting and weakness - stork feet.
Foot drop
Hammer toes - toe bend up at middle joint
Pes cavus

246
Q

Aetiology/Risk Factors of Spinal Muscle Atrophy

A

SMN1 gene mutation.
Affects babies

247
Q

Pathophysiology of Spinal Muscle Atrophy

A

SMN1 gene mutation causes congenital anterior horn atrophy.

248
Q

Clinical Presentation of Spinal Muscular Atrophy

A

LMND symptoms - flaccid paralysis, tongue fasciculations.
Symmetrical muscle weakness.

249
Q

Aetiology/Risk Factors of Myasthenia Gravis

A

Other autoimmune disorders such as DM, hashimoto’s.
Female gender more likely before 40 years.
Associated with thymic hyperplasia/cancer in Men

250
Q

Pathophysiology of Myasthenia Gravis

A

Autoimmune reaction against nicotinic Ach receptors.

Deposition of anti-acetylcholine receptor antibody complexes and complement proteins on the post-synaptic membrane.

Also presence of anti-muscle specific kinase (MuSK) antibodies - MuSK is a protein involved in synthesis of AchRs.

Results in receptor destruction and lack of cholinergic transmission.

251
Q

Clinical Presentation of Myasthenia Gravis

A

Muscular weakness - gets worse with use and improves with rest.

Diplopia & ptosis - extra-ocular muscles affected

Dysphagia, speech difficulties.

252
Q

Investigation of Myasthenia Gravis

A

Serology: Anti-AChR/Anti-MusK antibodies
Electromyography and nerve conduction studies

253
Q

Management of Myasthenia Gravis

A

FL: Acetylcholinesterase inhibitors e.g oral pyridostigmine.
SL: Steroids e.g oral prednisolone.

254
Q

Aetiology of Lambert-Eaton Syndrome

A

Associated with small cell carcinoma of the lung

255
Q

Pathophysiology of Lambert-Eaton Syndrome

A

Presence of pre-synaptic Ca channel antibodies.

256
Q

Clinical Presentation of Lambert-Eaton Syndrome

A

Limb weakness that improves with muscle use
Affects extremities first

Symptoms do not improve with pyridostigmine administration.

257
Q

Management of Lamber Eaton Syndrome

A

Prednisolone + IV immunoglobulins

258
Q

Aetiology of Duchenne’s Muscular Dystrophy

A

X-linked mutation in dystrophin gene.

259
Q

Clinical Presentation of Duchenne’s Muscular Dystrophy

A

Gowers sign - difficulty so usage of upper extremities to help get up.

Calf muscle hypertrophy - waddling gait.

Initial pelvic girdle muscle weakness that progresses superiorly.

260
Q

Complications of Duchenne’s Muscular Dystrophy

A

Dilated cardiomyopathy if before 5 years of age.

261
Q

What is a Tremor?

A

Involuntary, rhythmic oscillatory movement of a body part.

262
Q

Aetiology of Tremors

A

Physiological - anxiety, excitement, etc.
Drugs/toxins e.g alcohol, coffee
Metabolic - hyperthyroidism
Essential/resting tremors - Parkinson’s
Dystonic tremor
Functional tremor

263
Q

Clinical Presentation of Essential Tremor

A

Occurs upon movement/actions e.g lifting a cup.
Does not occur when at rest.
Responds to alcohol.
Is symmetrical

264
Q

Management of Essential Tremor

A

Anti-epileptics e.g primidone, gabapentin (CCB)
Beta blockers e.g propanolol.

265
Q

Clinical Presentation of Dystonic Tremor

A

Relatively similar to essential tremor.
More jerky movements
Variable axis - can be jerks in any direction.
Can be task specific such as writing

266
Q

Clinical Presentation of Functional Tremor

A

Distractibility - tremor increases when attention is paid to it.

Entrainability - tremor can synchronize with movement of another body part.

Whack-a-mole sign where there is systemic spreading of the tremor based on where examinations are done/attention is given.

Little finger of one hand is hyperextended.

267
Q

Clinical Presentation of Dystonia

A

Sustained or intermittent muscle contractions.

Worsened by voluntary actions and muscle overflow.

Can be specific to certain actions e.g running, playing guitar, etc.

Geste antagoniste - Certain actions or thinking of actions can settle the spasms

Lower limb dystonia is usually in those <21 years old.

268
Q

Features of Functional Dystonia

A

Functional Dystonia
Fixed limb at onset
Dystonia resistant to manipulation
Atypical botox response.
Pain - can follow minor injury.
Asymmetric facial spasms - cranial functional dystonia.

269
Q

Clinical Presentation of Chorea

A

Sudden irregular, flowing, variable movement.
People can be fidgety, clumsiness

270
Q

Aetiology of Chorea

A

Huntington’s chorea
SLE
Infections - HIV
Hyperthyroidism

271
Q

Clinical Presentation of Tics & Tourette’s Syndrome

A

Have a premonitory urge
Can be suppressed
Echolalia/echopraxia - copying what people say/do
Coprolalia/praxia - using obscene language/actions.

272
Q

Clinical Presentation of Functional Tics

A

Explosive onset
No premonitory urge
Not suppressible
Occurs at adolescence or later.

273
Q

Clinical Presentation of Myoclonus

A

Sudden, brief uncontrolled muscle contraction.

274
Q

Aetiology of Myoclonus

A

Physiological - hiccup, hypnic jerk when drifting off

Cortical - epilepsy (Fastest, distal muscles affected)

Subcortical - brainstem lesions (bilateral, synchronous, proximal muscles affected)

275
Q

Aetiology of Cauda Equina Syndrome

A

Lumbar disc herniation
Spinal tumour

276
Q

Clinical Presentation of Cauda Equina Syndrome

A

LMN lesion symptoms e.g hyporeflexia, flaccid paralysis.
Lower back pain, sciatica
Sphincter and urinary incontinence
Saddle anaesthesia - loss of peri-anal sensation.

277
Q

Investigation of Cauda Equina Syndrome

A

MRI spinal cord

278
Q

Management of Cauda Equina Syndrome

A

Neurosurgery

279
Q

Aetiology of Transverse Myelitis

A

SLE
EBV
MS

280
Q

Pathophysiology of Transverse Myelitis

A

Inflammation of the spinal cord causing swelling and loss of function of whole cross-section of the cord.

281
Q

Clinical Presentation of Transverse Myelitis

A

Progressive leg weakness
UMN injury signs e.g hyperreflexia,
Sensory loss below lesion

282
Q

Investigation of Transverse Myelitis

A

MRI spinal cord

283
Q

Management of Transverse Myelitis

A

Treat underlying cause
Steroids e.g prednisolone.

284
Q

Aetiology of Wernicke’s Encephalopathy

A

Vitamin B1 (thiamine) deficiency
Chronic alcoholism

285
Q

Pathophysiology of Wernicke’s Encephalopathy

A

Alcohol prevents phosphorylation of thiamine into it’s active form.

Alcoholic steatohepatitis can interfere with thiamine storage causing deficiency.

Thiamine is needed for ATP production within the brain through glucose/fatty acid metabolism.

286
Q

Clinical Presentation of Wernicke’s Encephalopathy

A

Ataxia
Confusion
Opthalmoplagia - weakness of eye muscles.

287
Q

Investigation of Wernicke’s Encephalopathy

A

FBC: Non-megaloblastic macrocytic anaemia if alcohol.

Can have deranged LFTS

288
Q

Management of Wernicke’s Encephalopathy

A

IV thiamine infusion, can be given with glucose.

In diabetic patients, normalise the thiamine first as lack of thiamine pyrophosphate can cause lactic acidosis.

289
Q

Complication of Wernicke’s Encephalopathy

A

Korsakoff’s syndrome
Presents with amnesia (anterograde and retrograde)
Confabulation - fabrication of stories to fill in memory gaps.

Sirpi's Phase 2A Medicine (13 decks)

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