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RW Neurology > Clinical Neurology > Flashcards

Clinical Neurology Flashcards

1
Q

What appears darker on CT scan, white matter or grey matter?

A

White matter is darker, as it is less dense due to the fatty myelin

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2
Q

What is used as artificial contrast in CT? And what can it be used to show?

A

Iodine, as it is dense in electrons. It can show an angiogram, then a venogram, then any disruption to BBB as it doesnt normally cross

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3
Q

What determines the contrast in CT and MRI?

A

CT = electron density; MRI = proton density

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4
Q

What are the advantages of CT over MRI and vice versa with neuroimaging?

A

CT shows better bone detail, fast, can be used with ICU/emergency equipment, better with stroke and head injury; however MRI shows better pathology contrast, multiples and no ionisation

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5
Q

Which areas of the brain are head injuries and contusions most commonly found?

A

At the junctions between lobes and hemispheres

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6
Q

What are T1 hyper intense MRIs (bright) best for?

A

Fat and the 4Ms (minerals, methemoglobin -subacute haematoma, melanin, mush)

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7
Q

What is Schizencephaly?

A

A large cleft forms in the cortex

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8
Q

What is Polymicrogyria?

A

Cortex in some areas is underdeveloped, with a smaller surface area so doesn’t have any gyri

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9
Q

What is the risk with any cortical abnormalities?

A

Seizures

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10
Q

What kind of inheritance is Duchenne’s Muscular Dystrophy?

A

X-linked recessive

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11
Q

What kind of inheritance is Huntington’s?

A

Autosomal dominant

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12
Q

How does curare cause paralysis?

A

It is a competitive antagonist of ACh. It therefore doesnt open the ion channel, preventing contraction and eventually stops respiration

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13
Q

How does Clostridium botulinum cause muscle paralysis?

A

Toxin cleaves presynaptic proteins involved in vesicle formation and block vesicle docking with the presynaptic membrane.

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14
Q

How does Lambert Eaton Myasthenic Syndrome cause muscle paralysis?

A

Antibodies to presynaptic calcium channels leads to less vesicle release

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15
Q

Where is the location of disorder in Myasthenia Gravis?

A

Post synaptic membrane of neuromuscular junction

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16
Q

What are fasciculations? What are their causes?

A

Visible, fast, fine, spontaneous twitches (e.g. eye twitch). May occur in healthy muscle – precitated by stress, caffeine, fatigue, or can occur in denervated muscle which become hyperexcitable.

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17
Q

What is myotonia?

A

Failure of muscle relaxation after use

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18
Q

*What are the 6 main types of muscle disorders?

A

*

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19
Q

What are some infective causes of muscle disorders?

A

Borrelia occurring as a result of Lyme disese in ticks; myalgic from viral infections

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20
Q

What are important aspects of examination of muscle?

A

Inspection (thin, wasting, fasciculations); palpation; Strength testing (power across joints); neck strength (flexion and extension - should never be able to over come these); core strength; fatiguability (ask them to repeat tasks several times then test again e.g. holding arms up or blinking)

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21
Q

Which system is used to grade muscle power?

A

MRC Muscle Power Grading (0 = no movement at all, 5 = full strength)

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22
Q

What is a normal adult ICP?

A

9-11 mmHg

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23
Q

What is the formula for Cerebral Perfusion Pressure (CPP)?

A

CPP = MAP - ICP (basically pressure coming up from the heart minus the pressure coming from the head pushing it back)

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24
Q

What CCP are you aiming for after head injury?

A

> 60mmHg (enough to perfect, but not too high an ICP to prevent perfusion)

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25
Q

What is global cerebral autoregulation?

A

Brain autoregulates the blood pressure to maintain constant CPP regardless of MAP

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26
Q

What is focal cerebral autoregulation?

A

Blood flow coupling to areas of high level of function

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27
Q

What constitutes a coma?

A

Do not open eyes, follow commands, speak. Equates to a GSC sum of 8 or less

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28
Q

What kills patients in coma with head injury?

A

Hypoxia, hypotension, raised ICP

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29
Q

What is post-concussive syndrome?

A

Poor concentration, poor memory, lethargy and headache

30
Q

In what context does acute neuronal injury occur and what is the classic appearance?

A

Hypoxia/ischaemia, causing ‘red neurons’

31
Q

What is the pattern of injury in acute neuronal injury?

A
  • Shrinking and angulation of nuclei
  • Loss of nucleolus
  • intensely red cytoplasm
32
Q

What is the axonal response to injury?

A

Degeneration of axon and myelin distal to the site of injury (Wallerian Degeneration) as well as cell body swelling and enlarged nucleolus due to increased protein synthesis

33
Q

What is the difference in axonal response to injury between central and peripheral NS?

A

In CNS there is axonal and myelin degeneration, whereas in the PNS the myelin is often preserved to provide a neural tube to aid regeneration

34
Q

When does simple neuronal atrophy occur?

A

It occurs in diseases of long duration, e.g. MS and AD

35
Q

When do sub-cellular alteration occur, and what occurs in each?

A

In neurodegernative conditions (levy bodies form); ageing (inclusions appear) and viral diseases (intranuclear and cytoplasmic inclusions)

36
Q

What is the most important histopathological indicator of CNS injury?

A

Gliosis (astrocytic response)

37
Q

What occurs in gliosis?

A

Undergo hyperplasia and hypertrophy, and get enlarged nuclei. In old lesions, nuclei become small and dark and lie in a dense net of processes (glial fibrils)

38
Q

Which cells are particularly sensitive to oxidative damage?

A

Oligodendrocytes (as they have a low anti-oxidant reserve)

39
Q

What is the ependymal cell response to injury?

A

Limited response, but ependymal granulation form as small irregularities on ventral surface

40
Q

What is the microglial response to injury, and what is the action of each type as inflammatory mediators?

A

Microglia proliferate and from aggregates around damaged tissues. M1 is pro-inflammatory and more chronic. M2 is anti-inflammatory and phagocytic (more acute)

41
Q

What is excitotoxicity and when does it occur?

A

Occurs in hypoxia and ischaemia, as energy failure causes a collapse on membrane potential and depolarisation, causes glutamate release and failure of glutamate re-uptake resulting in a glutamate storm and excitation. This causes huge influx of calcium causing several processes eventually resulting in apoptosis

42
Q

What is cytotoxic oedema, and when does it occur?

A

Dying cells accumulate water as osmotic ions move into the cell taking water with it - this can enhance other types of oedema. Occurs in intoxication and hypothermia

43
Q

What is ionic oedema and when does it occur?

A

First dysfunction of BBB, so Na crosses the BBB, driving chloride and therefore gradient causes water accumulation leading to swelling of the brain (worsened by cytotoxic oedema). Occurs with hyponatraemia and excess water intake (SIADH)

44
Q

What is vasogenic oedema and when does it occur?

A

Dysfunction of the BBB allows albumin to leak in an water follows. Occurs with trauma, tumours, inflammation, infection, encephalopathy etc

45
Q

What is haemorrhagic conversion?

A

So much disruption in BBB that RBCs can cross into the cellular space, and when these break down they become noxious

46
Q

Global hypoxic ischaemic damage

A

Systemic compromise to circulation so severe t cannot be compensated for by autoregulation eg. severe hypotension or cardiac arrest

47
Q

Focal hypoxic ischaemic damage

A

Restriction of blood flow to a localised area of the brain e.g. vascular obstruction

48
Q

Which areas of the brain are particularly affected by global ischaemic damage?

A

Watershed areas - areas at the periphery of two arterial territories, because they are the most distant from the heart and the least well supplied

49
Q

What symptoms would be caused by carotid artery disease?

A

Contra-lateral weakness or sensory loss

50
Q

Where would the weakness be localised in a lesion of the middle cerebral artery?

A

Contralateral face and arm

51
Q

Where would the weakness and sensory loss be localised in a lesion of the anterior cerebral artery?

A

Contralateral leg

52
Q

What would the symptoms be in vertebra-basilar artery disease?

A

Vertigo, ataxia, dysarthria, and dysphasia. Complex “brain stem syndromes”

53
Q

Hyaline atheroscerlosis

A

When vessels are less compliant, a larger perfusion pressure is required more prone to rupture and forming aneurysms

54
Q

Lacunar infarcts

A

Atheroma emboli occluding the small penetrating vessels, which damage deep structures such as basal ganglia, thalamus and internal capsule. Can accumulate and cause multi-infarct dementia

55
Q

What is Hypertensive encephalopathy and why does it occur?

A

Fluid leaks across the BBB causing global cerebral oedema, tentorial and tonsillar herniation, petechiae and arteriolar fibrinoid necrosis. Occurs because hypertension saturates the upper limit of auto regulation and BBB can no longer resist the pressure.

56
Q

What is amyloid angiopathy, and in which situations does it occur?

A

Beta amyloid forms tight sheets which are deposited in the cerebral and meningeal vessels, which are less complaint and can rupture forming lobar intracerebral haemorrhages. Occurs in Alzheimer’s as well as old age.

57
Q

What are the hallmark characteristics of MS?

A

Separation in time (relapsing episodes) and space (asymmetric lesions in different areas of the CNS)

58
Q

What characterises neurodegenerative diseases?

A

Progressive loss of neurons affecting functionally related neuronal groups

59
Q

What is the main difference between Lewy Body Dementia and Alzheimer’s?

A

Lewy body dementia has hallucinations and also a fluctuating course

60
Q

What is the triad of disturbances in Huntington’s disease?

A

Emotional, cognitive and motor disturbance

61
Q

How does the body compensate with raised ICP?

A

Some blood and/or CSF leaves the cranial vault, after this is exhausted venous sinuses are flattened and there is little or no CSF

62
Q

What is the normal volume of CSF?

A

120-150ml (500ml produced a day)

63
Q

Hydrocephalus ex vacuo

A

Dilatation of the ventricular system and a compensatory increase in CSF volume secondary to a loss of brain parenchyma (e.g. in Alzheimer’s Disease)

64
Q

What are the effects of raised ICP?

A

Midline shift, compression of cranial nerves, herniations, impaired blood flow, reduced LOC

65
Q

Is cerebral metabolism increased or decreased in head injury?

A

Decreased, blood flow is frequently uncoupled from metabolic requirements and there is a frequent loss of neurovascular pressure autoregulation

66
Q

What urgent investigation should you do with a patient who has a headache that wakes them up plus vomiting?

A

Fundoscopy

67
Q

What is the difference between radiculopathy, plexopathy and peripheral neuropathy?

A

Radiculopathy: problem occurs at the nerve root(lets)
Plexopathy: an entire plexus is affected e.g. brachial or lumbar
Peripheral neuropathy: damage to the nerve further along its course

68
Q

What is the difference between tics, tremors, dystonia, myoclonus and chorea?

A 
Tremor = rhythmic sinusoidal oscillation 
Tics = brief, sudden and suppressible movements and/or sounds
Dystonia = involuntary and sustained muscle contraction often causing abnormal postures
Myoclonus =  brief, electric-shock-like jerks e.g. hiccups or when falling asleep
Chorea = brief movements flitting from one body part to another - dance-like
69
Q

What are important relieving and exacerbating factors with headache?

A

Relieving: Posture (lying down, headache behaviour
Exacerbating: Posture, valsalva (coughing, straining etc), diurnal variation

70
Q

What are red flags with headaches?

A
  • New onset headache >55
  • Known/previous malignancy
  • Immuno-suppressed
  • Early morning headache (raised ICP)
  • Exacerbation by valsalva (coughing, sneezing-raise intracranial pressure)

RW Neurology (3 decks)

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