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Neurology and psychiatry > Brain pathology + other disorders > Flashcards

Brain pathology + other disorders Flashcards

1
Q

What 3 ways can infection enter the brain?

A
  • Direct spread from middle ear infection or basilar skull fracture
  • Blood borne (sepsis, infective endocarditis)
  • Iatrogenic (lumbar puncture, surgery)
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2
Q

What is meningitis the inflammation of?

A

The leptomeninges- pia and arachnoid not dura.

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3
Q

What organism is most likely to cause meningitis in a neonate?

A

e coli or l. monocytogenes

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4
Q

What organism is most likely to cause meningitis in a 2-5 yr old?

A

H. influenza

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5
Q

What organism is most likely to cause meningitis in a >30 yr old?

A

s. pneumonia

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6
Q

Give 4 complications of meningitis

A
  • Brain damage due to swelling and raised ICP
  • Death due to brain damage
  • Cerebral abscess (needs surgical treatment)
  • subdural empyema
  • epilepsy
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7
Q

What causes chronic meningitis?

A

M. tuberculosis - granulomatous inflammation is seen

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8
Q

What is the result of chronic meningitis?

A

Fibrosis, leading to entrapment of nerves leading to cranial nerve palsies

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9
Q

What is the most likely cause of temporal lobe encephalitis, spinal cord motor neurone and brain stem encephalitis?

A

Temporal lobe= a herpes virus (eg cytomegalovirus)
Spinal cord motor neurone= polio
Brain stem= rabies

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10
Q

How does encephalitis present?

A

Headaches, nausea, photophobia etc, usually in an immunocompromised or herpes pt

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11
Q

How do prions cause disease?

A

The mutated prions cause other normal prions to change conformation to be like the mutated ones, which aggregate and accumulate in neurones and cause neuronal death. This gives the brain a spongey appearance.

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12
Q

Give 2 examples of prion diseases?

A

varient cretuzfelt jacob disease, scapie in sheep, BSE in cow, Kuru in tribes of new guinea

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13
Q

What are the 4 types of dementia? Give in order of prevelance

A
  • alzheimers (50%)- can be sporadic or famillial and early or late (late sporadic most common)
  • vascular dementia (20%)
  • lewy body
  • frontotemporal dementia
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14
Q

Describe the pathogenesis of alzheimers dementia?

A

Tau protein (which normally binds and stabilises microtubules) becomes hyperphosphylated and so aggregates and causes neuronal cell death. The dead neurones full of tau aggregate to form senile plaques. Amyloid is deposited in the vessels at the centre of the plaques. This leads to loss of cortical neurones, which causes the decline in brain function.

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15
Q

What is the most common type of brain tumour in adults?

A

meningioma

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16
Q

What is the most common malignant brain tumour?

A

astrocytoma

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17
Q

Define dementia?

A

progressive decline in higher cortical function leading to a global impairment of memory, intellect and personality which effects the individuals ability to cope with activities of daily living.

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18
Q

Give 3 reversible causes of dementia?

A

depression, trauma, vitamin deficiency, alcohol, thyroid disorders.

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19
Q

Give 4 presentations of dementia?

A
  • memory deficit
  • behavioural- altered personality, disinhibition, labile emotions, wandering
  • physcial- incontinence, reduced oral intake, difficulty swallowing, apraxia (difficulty with motor planning)
  • language disorder- difficult understanding, anomic aphasia (loss of word retreival)
  • visuospatial disorder- unable to identify visual and spatial relationships between objects
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20
Q

How would dementia be investigated?

A
  • history + collateral history +mini mental state exam
  • full neurological exam
  • blood tests for reversible causes- B12, TFTs
  • CT/ MRI head
  • memory clinic follow up
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21
Q

What may a CT of dementia show?

A
  • may be normal

- may show ventricle dilation and generalised atrophy

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22
Q

What may an MRI of dementia show?

A

Axial and coronal sections of T1 may show hippocampus atrophy

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23
Q

How can you differentiate between delirium and dementia?

A

CAM score of >2= delirium:

  • Acute change or fluctuating mental status
  • altered consciousness (hypo or hyperactive)
  • inattention (can they count from 20-0)
  • disorganised thinking
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24
Q

Describe the pattern of mental status decline over time for alzheimers disease?

A

Generally steady decline as time goes on

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25
Q

Give 2 microscopic changes seen in alzheimers?

A
  1. amyloid beta plaques

2. neurofibillary tangles (tau protein aggregates)

26
Q

Describe the 3 stages of alzheimers

A
  • mild: lasts 2-4 yrs, minor memory loss and learning difficulty, pt may hide it
  • moderate: lasts 2-10 yrs, withdrawal, confusion, anger, anxiety, frustration start to happen, generally present to GP in this stage as care is needed
  • Severe: lasts 1-3 yrs, short and long term memory loss, loss of bodily functions, forget to feed themselves, violent episodes common
27
Q

Why does dementia shorten life span?

A

They loose ability to care for themselves, which impacts immune system and reduced ability to recover from infections, falls etc.

28
Q

Describe the pattern of mental decline seen in lewy body dementia?

A

mental capacity can rise and fall, some days/ months good and some bad, generally downward trend

29
Q

Describe the microscopic changes seen in lewy body dementia and how this is different to parkinsons?

A

Lewy bodies found in cortex and substantia nigra, in parkinsons the lewy bodies are only found in the substantia nigra.

30
Q

Give 3 features of lewy body dementia?

A
  • fluctuations in degree of cognitive impairment
  • parkinsons symptoms
  • visual hallucinations
  • frequent falls
31
Q

Describe the pattern of mental function decline of vascular dementia

A

Step wise decline

32
Q

What is the pathogenesis of vascular dementia?

A

Arteriosclerosis of blood vessels supplying the brain= diffuse small vessel disease resulting in decreased blood supply to parts of the brain.

33
Q

How is vascular dementia managed?

A

reducing cardiovascular risk - treat hypertension, high cholesterol etc

34
Q

What are the frontotemporal dementias?

A

A group of conditions with similar presentations but differnt pathologies:

  • frontotemporal lobar degeneration with tau pathology
  • picks disease
  • famillial tauopathy
35
Q

Give 3 signs of frontotemporal dementia?

A

social behaviour and personality changes, impaired judgement and disinhibition, speech output falls eventually to state of mutism

36
Q

Give 1 pharmacological treatment of dementia?

A

Acetyl cholinesterase inhibitors can work for a few months in some pts- eg rivastigmine, donepezil
NMDA blockers such as memantine can also help

37
Q

Give 3 non pharmacological treatments of dementia?

A
  • therapies (babies and puppies)
  • memory aids (orientation boards, remembrance therapy, life stories)
  • social care (risk assessment, care needs, mental capacity act)
38
Q

What is epilepsy?

A

A neurological disorder marked by sudden recurrent episodes of sensory disturbance, loss of consciousness or convulsions, associated with abnormal electrical activity in the brain

39
Q

What is a seizure?

A

sudden, irregular discharge or electrical activity in the brain causing physical manifestations such as sensory disturbance, unconsciousness or convulsions

40
Q

What is an aura?

A

A perceptual distubance experienced by some prior to a seizure. eg a strange light, unpleasant smell, confusing thoughts. They tend to reoccur so can be used as warnings

41
Q

what is status epilepticus?

A

seizures occurring continuously without recovery of consciousness in between lasting up more than 5 mins. Tend to be due to head injury, stroke, infections, tumours, alcohol withdrawl.

42
Q

What is a partial seizure?

A

Where the electrical activity is confined to one part of the brain

43
Q

Whats the difference between a simple and complex partial seizure?

A

simple partial seizures= remain conscious and awareness

complex partial seizures= lose awareness +/- consciousness

44
Q

What is the most common cause of partial seizure and what is commonly experienced (5)?

A

Temporal lobe epilepsy- usually due to early injury to the brain due to strokes, head injuries, infections etc.
Can lead to visual or verbal memory loss, emotional distubance, hallucinations, lipsmacking and auditory dysfunction

45
Q

What is the second most common type of partial seizure and what is commonly experienced (3)?

A

frontal lobe epilepsy. Often get abnormal movements, dysphasia (speech arrest) and behaviour change (psychosis, depression, personality disorders)

46
Q

What is a tonic clonic seizure? Other than epilepsy, what could cause one?

A 
Muscle tensing (tonic) and convulsions (clonic- rhythmic  jerking movements). 
May also be caused by ovulation, stress, head injury, stroke, hypertension, diabetes, fatigue.
47
Q

Describe an absence seizure?

A

The pt day dreams// stops all conscious functions momentarily then carries on as if nothing happened

48
Q

What is a myoclonic seizure?

A

brief shock like muscle jerks, pt does loose consciousness for event but so brief they appear conscious

49
Q

What is an atonic seizure? What syndrome do they indicate?

A

‘without tone’- drop attacks. tend to fall over or drop head backwards if sitting down. may be as brief as a few seconds but typically >15s. Tend to be rarer and indicate lennox- gasthaut syndrome.

50
Q

What is a tonic seizure?

A

brief increase in muscle tone/

51
Q

What are the differentials for epilepsy?

A 
V: stroke, tia
I: abcess, meningitis
T: haemorrhage, head trauma
A: SLE
M: hypoxia, electrolyte imbalance, hypoglyaemia, thyroid dysfunction 
I: drugs, alcohol withdrawal
N: tumour
52
Q

What is a post ictal state?

A

N+ V, drowsiness, reduced consciousness state for 1-24 hrs after a seizure.

53
Q

What investigations are required for epilepsy?

A
  • EEG: try inducing a seizure w/ hyperventilation
  • MRI: excludes differentials
  • ECGs: excludes cardiac causes of syncope
54
Q

How is a seizure managed?

A

ABCDE

Benzodiazepam, then more if still going after 5 mins, then phenytoin after 10-15 then call ITU

55
Q

What are the rules concerning epileptics driving?

A

No driving till one yr seizure free. If due to med change, need 6 months free. If seizures when asleep or dont affect consciousness the DVLA assesses case by case.

56
Q

Describe pathogenesis of MS?

A

oligodendrocytes are marked by antibodies from B cells, macropahges will engulf them and leave behind scar tissue

57
Q

What CT changes can be seen in MS?

A

Hyperdense (white) plaques in brain

58
Q

Give 3 examples of signs and symptoms of MS?

A 
Double vision (CNIII lesion)
Vision loss (CNII lesion)
Depression 
Shooting pains in cheeks (CNV)
Tinnitis, vertigo, hearing loss (CNVIII)
Facial weakness (CNVII)
Impotence
Shooting pains
Loss of pain sensation
59
Q

What is an arteriovenous malformation?

A

An abnormal connection between arteries and veins, bypassing the circulatory system, can occur anywhere but commonly affect CNS.

60
Q

When to arteriovenous malformations become symptomatic?

A

When very large (cause headaches, epilepsy) or rupture leading to stroke like symptoms.

61
Q

What is the name for the dilated vein in an arteriovenous malformation?

A

A nidus- dilates as cant cope with the high pressure. Can often be heard (by pt or through stethoscope) as creates turbulent blood flow.

Neurology and psychiatry (8 decks)

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