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Conditions + definitions > Neuro 5 > Flashcards

Neuro 5 Flashcards

1
Q

What are the ischaemic causes of stroke?

A 
Large artery atherosclerosis
Cardioembolic
Small artery occlusion
Undetermined
Rare causes - arterial dissection, venous sinus thrombosis
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2
Q

What are the haemorrhagic causes of stroke?

A

Primary intracerebral haemorrhage
Secondary haemorrhage
>Subarachnoid haem
>Arteriovenous malformation

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3
Q

How are lipid levels related to stroke?

A

An increase in serum lipids levels leads to an increase in plasma level of LDL
Resulting in greater amounts of LDL in arterial wall and atheroma
HT, cigarette + diabetes all contribute

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4
Q

What are the symptoms of ACA occlusion?

A

Contralateral:
>Paralysis of foot/leg
>Sensory loss over foot/leg
>Impairment of gait/stance

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5
Q

What are the symptoms of MCA occlusion?

A 
Contralateral:
>Paralysis of face/arm/leg
>Sensory loss face/arm/leg
>Homonygmous heminaopia
>Gaze paralysis contralateral
Aphasia if on dominant (left) side
Unilateral neglect and agnosia if non dominant stroke (norm right)
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6
Q

What are the symptoms of a left hemisphere stroke?

A

Left Hemiplegia,
Left homonymous hemianopia,
dysphasia

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7
Q

What are the symptoms of a Right hemisphere stroke?

A

Left hemiplegia, homonymous hemianopia
Neglect syndromes
Visual, sensory agnosia, anosagnosia (denial of hemiplegia), prosopagnosia (failure to recognise faces)

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8
Q

What are the lacunar stroke symptoms?

A

Devoid of cortical signs
Pure motor or sensory stroke
Dysarthria (clumsy hands)
Ataxic hemiparesis

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9
Q

What are the posterior circulation stroke symptoms?

A

Brain stem, cerebellum, thalamus, occipital + medial temporal lobes affected
Coma, vertigo, nausea, vomiting, cranial nerve palsies, ataxia
Hemiparesis, hemisensory loss
Crossed sensorimotor defcits
Visual field deficits

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10
Q

What are the criteria for TPA use?

A

Less than 4.5 hours since onset
Disabling neurological deficit
Symptoms present for greater than 60mins
Consent is obtained

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11
Q

What are teh exclusions for TPA use?

A 
Anything increasing possibility of haemorrhage 
>Blood on CT
>Recent surgery
>Recent episodes of bleeding
>Coagulation problems
BP > 185 systolic, >110 diastolic
Glucose <2.8 or > 22
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12
Q

What is the secondary prevention for stroke?

A 
Antihypertensives
	Antipolateltes
	Lipid lowering agents
	Warfarin for AF
Carotid endartectomy
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13
Q

What are differentials to stroke?

A 
Posti-ictal states 
	Hypoglycaemia
	Intracranial masses
	Vestibular disease
	Bell's palsy
	Functional hemiparesis
	Migraine
Demented patients with UTIs
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14
Q

What is dementia?

A

Progressive impairment of multiple domains of cognitive function in alert patient leading to loss of acquired skills and interferences in occupational and social role
Common and increasing prevalence, incidence 200/100000

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15
Q

What are the causes of late onset dementia?

A

Alzheimers 55%
Vascular 20%
Lwey body 20%
Other 5%

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16
Q

What are the causes of early onset dementia?

A 
Alzheimers 33%
Vascular 15%
Frontotemporal 15%
Other 33%
>Toxic (Alcohol), 
>genetic (huntingtons), 
>infection (HIV, CJD), 
>inflammatory (MS)
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17
Q

What is late onset dementia vs early dementia?

A

Late onset is after 65 years old

Early onset any time before that

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18
Q

What are the treatable causes of MS?

A

Vitamin deficiency - B12
Endocrine - thyroid disease
Infective - HIV, syphilis

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19
Q

How do you diagnose dementia?

A

History (independent witness) - type of deficit, progression, FH, risk factors
Exam - cognitive function, neurological, vascular
Investigations - routine bloods, CT/MRI
Others - CSF, EEG, functional imaging, genetics

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20
Q

How do you examine cognitive function?

A

Various domains - memory, attention, language, visuo-spatial, behaviour, emotion, executive function apraxias, agnosias
Screening tests - mini-mental (MMSE), Montréal (MOCA)
Neuropsychological assessment

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21
Q

What are the indicators for specific types of dementia?

A 
type of cognitive deficit
speed of progression
>rapid progression (CJD)
>stepwise progression (vascular)
other neurological signs
>abnormal movements (Huntington's)
>parkinsonism (Lewy body)
>Myoclonus (CJD)
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22
Q

What are the types of alzheimers disease?

A

Tempo parietal dementia

frontotemporal dementia

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23
Q

What is tempoparietal dementia?

A

early memory disturbance
language and visuospatial problems
personality preserved until later

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24
Q

What is frontemporal dementia?

A

early change in personality/behaviour
often changing eating habits
early dysphasia
memory/visuospatial relatively preserved

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25
Q

What are the non-pharmacological treatments for dementia?

A

information support
Occupational Therapy
social work/support/respite/placement
voluntary organisations

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26
Q

What are the pharmacological treatments for

Alzheimer’s disease?

A 
Cholinesterase inhibitors (cholinergic deficit)
NMDA antagonist (memantine)
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27
Q

What are the examples of cholinesterase inhibitors?

A

Donepezil, rivastigmine, galantamine

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28
Q

Name an NMDA inhibitor.

A

memantine

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29
Q

What is parkinsonism?

A 
Bradykinesia
rigidity
tremor
postural instability
pathology in basal ganglia – predominately dopamine loss
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30
Q

What are the types of Parkinson’s disease?

A

idiopathic,
drug induced (dopamine antagonist),
vascular Parkinson,
Parkinson’s plus syndromes (multiple system atrophy, progressive supra-nuclear policy

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31
Q

How do you diagnose Parkinson’s?

A

Bradykinesia plus one or more of
>tremor rigidity
>postural instability

no other cause
slowly progressive
supported by asymmetric rest tremor, good response to deepening replacement

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32
Q

What are the complications of Parkinson’s? (Drugs)

A

motor fluctuations – levodopa wears off
dyskinesia’s – in voluntary movements
psychiatric – hallucinations, impulse control

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33
Q

What are the non-drug complications of Parkinson’s?

A 
depression
		dementia
		autonomic (BP, bladder, bowel)
		speech, Swallow
balance
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34
Q

How do you treat Parkinson’s?

A

prolong levodopa half life
>MAOB inhibitors,
>COMT inhibitor, slow-release)

add dopamine agonist
continuous infusion (Apomorphine, Duodopa)
functional neurosurgery (deep brain stimulation)
Allied health professionals
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35
Q

What is the choroid plexus responsible for, where is it found?

A

Responsible for production of CSF
Mostly floor of lateral ventricles
Some in roof of 3rd/4th

36
Q

What is the flow pathway for CSF?

A 
Lateral ventricles
	Foramina of Munro 
	3rd Ventricle
	Aqueduct of Sylvius
	4th Ventricle
	Foramen of Magendie (medial, x1) &amp; Foramen of Luschka (lateral, x2)
	Subarachnoid spaces
	Arachnoid granulations
	Dural venous sinuses
37
Q

What are teh clasifications of hydrocephalus?

A

Obstructive - blockage of flow from ventricles

Communicating - block at level of arachnoid granulations

38
Q

What are the congenital causes of hydrocephalus?

A

Chiari malformation
Aqueductal stenosis
dandy walker malformation

39
Q

What are the acquired cases of hydrocephalus?

A 
meningitis
		post haemorrhagic
		neoplastic
		Post op
		Cerebellar stoke
		post-traumatic
40
Q

What are the clinical features of hydrocephalus in infants?

A 
Cranial enlargement – regular measurements of circumference needed
Splaying of cranial sutures
Irritable, poor feeding
Fontanelles full &amp; bulging
Engorged scalp veins
Abducens (VI nerve) palsy 
Perinaud’s syndrome:  
‘sunsetting’ (upward gaze palsy)
Convergent nystagmus
Eyelid retraction
Exaggerated reflexes
Respiratory problems
41
Q

What are the clinical features of hydrocephalus in adults and children?

A 
Increased ICP 
Headaches 
>worse in the morning, worse on cough/ straining
Papilloedema
Visual disturbances
Gait abnormality
Loss of upgaze or abducens palsy
Impaired consciousness
42
Q

What is the medical treatment of hydrocephalus?

A

may help as a temporising measure
Acetazolamide (carbonic anhydrase inhibitor)
>Reduces CSF production from choroid plexus

43
Q

What are the surgical measures for managing hydrocephalus?

A 
In emergency situation – EVD (external ventricular drain)
Eliminating obstruction
CSF diversion
>3rd Ventriculostomy
>Shunt insertion
44
Q

What are the possible complications of shunts?

A 
Over-drainage
>low pressure headaches,
>subdural haematoma
Under-drainage
Blockage
Infection 
Disconnection
Seizures
Distal end problems: 
>Abdominal hernias (VPS)
>Cardiac arrhythmias (VAS)
45
Q

What is ETV?

A

Endoscopic 3rd ventriculostomy (ETV)
Creating a fistula between 3rd ventricle and subarachnoid spaces / basal cisterns
Only works for non-communicating hydrocephalus

46
Q

What is normal pressure hydrocephalus?

A 
A potentially reversible dementia
Classical triad
>Dementia
>Gait disturbance (magnetic gait)
>Urinary incontinence
Age >60

‘Normal’ pressure on LP – diagnostic challenge
Improvement after shunt

47
Q

What is idiopathic hydrocephalus?

A 
BIH / pseudotumour cerebri
	Raised ICP without obvious cause
	 Typical patient is young obese female
	Often present with headaches &amp; visual disturbances – papilloedema
Patients will go blind without treatment
48
Q

How do you treat idiopathic hydrocephalus?

A

Lose weight!! (need to lose 6%)
Medical - acetazolamide
CSF diversion – VP or LP shunt
Optic nerve sheath fenestration

49
Q

What are the indications for lumbar puncture?

A

Obtain CSF for analysis
>Rule out bacterial or viral infection
>Measure for blood breakdown products (SAH)
>Measure protein load
>Test for the weird and wonderful
Measurement of pressure (intracranial pressure (ICP))
CSF drainage for raised pressure
Diagnostic test for Normal Pressure Hydrocephalus

50
Q

What are the risks of lumbar puncture?

A 
Bleeding
		Infection
		Nerve root injury
		Retroperitoneal / intra-abdominal injury
		Brainstem herniation
51
Q

What is the CSF like in meningitis?

A

Cloudy, turbid
WBC - lots!! – mostly polymorphs
Protein >1g/l
Glucose - low

52
Q

What causes CSF to be yellow?

A 
Xanthochromic
>Yellow due to blood breakdown products
>Most commonly seen in SAH
>In patients with suspected SAH based on history – with a normal CT scan – CSF spectrophotometry used to detect blood breakdown products (bilirubin)
>>Positive only after 12hrs
>>Persists for 3 weeks
53
Q

What are the types of dopaminergic drugs?

A

Dopamine precursor

Dopamine agonists

54
Q

What are examples of dopamine precursors?

A

Levodopa

55
Q

What are the examples of dopamine agonists?

A

Bromocriptine, pergolide
Ropinirole
Pramiexole
Apomorphine

56
Q

What eznyme inhibtors are useful in Parkinson’s?

A

Peripheral AAAD inhibitors

MOAB, COMT inhibitors

57
Q

What are peripheral AAAD inhibitors?

A

benserazide

Reduce peripheral side-effects of levodopa, allowing greater amount to reach CNS

58
Q

What are MOAB/COMT inhibtors?

A

MOAB - selegine
COMT - entacapone
Reduce metabolism of dopamine and so increase effectiveness of levodopa

59
Q

How do dopaminergic drugs affect Parkinson’s?

A

Improve parkinsons (rigidity + bradykinesia)
Fail to help “midline” features (dysathria, balance, cognition)
Worsen or cuse (Nausea, vomiting, psychosis)

60
Q

How do dopamine antagonists affect parkinson’s?

A

Improve (nausea, vomiting, psychosis)

Worsen/cause parkinsons (rigidity + bradykinesia)

61
Q

What is domperidone?

A

Dopamine antagonist that doesn’t cross the blood-brain barrier
Antiemetic
No antipsychotic properties
Relatively safe in PD
Has permitted therapeutic use of apomorphine

62
Q

What drugs can cause dyskinesias?

A 
Dopaminergic drugs (may cause dyskinesias - eg chorea)
DA antagonists - may cause parkinsonism
63
Q

What is hypocondriasis?

A

Preoccupation with disease + fear of illness
Persistent belief od unidentified disease
Requests for repeated reassurance/investigation

64
Q

What is somatisation disorder?

A

Example of abnormal illness behaviour
Chronic, onset before 30
Multiple unexplained physical symptoms

65
Q

What is conversion disorder?

A

“hysteria”
Loss of function of a body part
Signs mimic neurological disease + inconsistent
Patient not conscious of mechanisms, information from functional imaging

66
Q

What is malingering?

A

Inconsistent signs, may mimic neurological disease

Patient conscious of mechanisms

67
Q

What is chronic fatigue syndrome?

A

Chronic
Multiple physical symptoms - fatigue, arthralgia, myalgia
May overlap with other syndromes - eg fibromyalgia, chronic pain
Worse after exertion

68
Q

What is non-epileptic attack disorder?

A

Attacks look like epilepsy but not caused by abnormal electrical activity in the brain
Drug resistant
Abuse or neglect in childhood risk factor
Associated with anxiety, depression and post traumatic stress disorders

69
Q

How do you manage unexplained symptoms?

A 
Exclude physical disease
Carry out essential investigations, ovoid repeated ones
Psychiatric assessment
Explanations to patient
Consider anti-depressants
Consider cognitive behaviour therapy.
70
Q

What is post traumatic amnesia?

A

Period of recovery following traumatic brain injury
Disorientation - unable to locate themselves in time/space
Anterograde amnesia - inability to remember new events/experiences ocured after brain injury

71
Q

What should a cognitive function clinical interview entail?

A

Test memory - new learning in daily life
Language - word finding, errors, poor understanding etc
Processing speed - slowed down, long responses
Attention/concnetration
Executive functioning - difficulty making decisions
Personality - behaviour changes
Insight
Visual spatial - route finding etc

72
Q

What are the clinical features of spinal cord disease?

A

Pain - local or referred
Sensory - pins & needles, tingling (paresthesia) and numbness
Proprioception and temperature appreciation
Motor - weakness or complete plegia
Deformity

73
Q

What does cord compression lead to?

A 
Upper motor features
>Weakness
>Increased tone
>Increased reflexes
>Upgoing plantar response
>Clonus
74
Q

What does peripheral nerve root compression lead to?

A 
Lower motor features
>Wasting of muscle
>Fasciculation
>Weakness
>Decreased tone
>Decreased reflexes
>Plantar response - decreased or absent
75
Q

What are the common causes of degenerative spinal disease?

A 
Cervical spodylosis
>Myelopathy, radiculopathy
Lumbar spondylosis
>Radiculopathy
>Cauda equina syndrome
Spinal trauma
76
Q

What is cauda equina syndrome’s triad?

A

> Bilateral leg pain
Bladder +/1 bowel symptoms
Saddle sensory symptoms

77
Q

What are the features of carpal tunnel syndrome?

A

Pain worse at night
Pareatheisa/numbness
Median nerve compressed at wrist resulting in the numbness/pain

78
Q

What are the sudden onset long term neurological conditions?

A

Acquired brain injury
Spinal cord injury
Stroke

79
Q

What are the intermittant causes of long term neurological conditions?

A

Epilepsy

Early stages of MS

80
Q

What are the progressive causes of long term neurological diseases?

A

Motor neurone disease
Parkinsons
Later stages of MS

81
Q

What are the stable causes of long term neurological conditions?

A

Post-polio syndrome
Cerebral palsy
Spina bifida

82
Q

What are some other long term neurological conditions?

A

Guillain barre syndrome
Muscle diseases
Hereditary spastic paraparesis
Huntingtons

83
Q

What is spasticity?

A

Motor disorder characterised by velocity dependent increase in stretch reflexes with exaggerated tendon jerks
Disordered sensoriomotor control resulting from UMN lesion, presenting as intermittent or sustatined inoluntary activation of muscles

84
Q

What are the complications of spasticity?

A 
Poor seating and lying positions
	Sleep difficulties and fatigue
	Dressing and hygiene issues
	Pain, spasms and associated reactions
	Communication and feeding problems
	Pressure sores and contracture
	Poor self-image and relationship issues
85
Q

How do you manage spasticity?

A 
Prevention,Prevention and Prevention!
	Multidisciplinary team approach
	Physical therapy
	Exclude exacerbating factors
	Oral antispasticity agents
	Focal treatment with Botulinum toxin
	Drug Treatment not always necessary!
86
Q

What determines the severity of a head injury?

A

GCS,
length of loss of consciousness
post-traumatic amnesia are important

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