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All conditions - Year 3 > Neuroscience > Flashcards

Neuroscience Flashcards

1
Q

Name 5 symptoms of Bell’s Palsy

A 
Unilateral Facial Weakness 
Ear Numbness 
Ear Pain 
Decreased Taste
Hypersensitivity to sounds (Hyperacusis)
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2
Q

Name 2 risk factors for Bell’s Palsy

A

Pregnancy x3

Diabetes x5

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3
Q

Name 5 general symptoms of a 7th Nerve Palsy

A 
Dry eyes 
Unilateral sagging of the mouth 
Drooling 
Food trapped between gum and cheek 
Speech difficulty
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4
Q

Name 4 possible complications of Bell’s Palsy

A

Dry eyes
Sagging eyelids
Synkinesis
Crocodile tears

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5
Q

What is the common and most benign CNS tumour

A

Astrocytoma

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6
Q

What is the most aggressive CNS tumour

A

Glioblastoma

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7
Q

What is the ideal way to investigate CNS tumours

A

CT head is 1st Line

MRI actually has higher sensitivity

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8
Q

What is the cardinal presentation of Cluster Headaches

A

Unilateral excruciating orbital/temporal pain - Usually nocturnal

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9
Q

Name 4 risk factors for Cluster Headaches

A

Male sex
Head injury
Smoking
Alcohol - Common trigger

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10
Q

What are the possible associated symptoms of Cluster Headaches

A 
Over stimulation of PNS
Lacrimation 
Rhinorrhoea 
Miosis/Ptosis 
Facial Oedema 
Agitation

N+V
Phono/Photophobia

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11
Q

What are the diagnostic criteria for Cluster Headaches

A

International headache society-3b criteria
A - 5 headaches + satisfying B-E
B - Excruciating unilateral orbital/temporal pain lasting 15 - 180 minutes if left untreated.
C - At least 1 PNS associated symptom
D - Multiple headaches occurring a minimum of 1 every other day lasting 15-180 minutes each. Remission periods between attacks
E - Not attributed to another disorder

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12
Q

What are the 4 main subtypes of Dementia

A

Alzheimer’s (50%) -
Vascular (25%) - Cumulative effect of many small strokes
Lewy body (15%) - Fluctuating cognitive impairment, detailed visual hallucinations, later parkinsonism
Fronto-temporal (5%) - Executive impairment and personality changes
Parkinson’s disease dementia - Parkinson’s disease predates dementia

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13
Q

What are causes of reversible Dementia and what are investigations to test for these

A 
Hypothyroidism - High TSH
B12 and folate deficiencies
Thiamine deficiency
Hypocalcaemia
Subdural haematoma - CT/MRI
Normal pressure hydrocephalus - CT/MRI

Delineate subtypes - Functional Imaging
EEG

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14
Q

What are symptoms of Alzheimer’s Dementia

A

All dementias: Memory loss
Confusion, Apraxia, Aphasia
Later disease: Wandering, Disorientation, Psychiatric and Behavioural problems

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15
Q

How can you differentiate Alzheimer’s Dementia from the main other types

A

Vascular: Stepwise decline after a vascular event
Lewy body: Fluctuating levels of consciousness, hallucinations, sleep disorders, falls and parkinsonian features
Parkinson’s disease dementia: Parkinson’s disease predates dementia
Fronto-temporal: Behavioural changes (Disinhibition or apathy) and language disturbances

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16
Q

What are the main causes of Encephalitis

A

Viruses are the main cause - Most commonly HSV infection. Other viruses include arbovirus worldwide

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17
Q

Name 4 risk factors for Encephalitis

A

Immunodeficiency
Body fluid exposure
Organ transplantation
Bites

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18
Q

What are the signs and symptoms in Encephalitis

A

Fever
Headache
Altered mental state
Seizures

+ Other meningitis symptoms (Neck stiffness, Vomting)

Focal neurological
Raised ICP
Psychiatric symptoms

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19
Q

What are the main investigation findings of Encephalitis

A

Bloods - Blood cultures
CT - Do before LP
LP - Increased Proteins, Lymphocytes and decreased glucose. Send CSF for viral PCR
EEG - Diffuse abnormalities

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20
Q

Name 6 causes of Epilepsy

A

Most idiopathic

Developmental
Head injury
Cranial surgery - Cortical scarring
Space occupying lesion
Cerebrovascular event
Genetic disease
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21
Q

What is the major cause of Extradural haemorrhage

A

Trauma to the pterion causing middle meningeal artery damage

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22
Q

What are the early and late signs of Extradural haemorrhages

A

Early signs
Headache
Immediate fluctuating consciousness before a lucid interval (6-8hrs)

Late signs
Rapid deterioration after regaining consciousness (Falling GCS)
Bradycardia + Hypertension (Rising ICP)
Vomiting
Confusion
Seizures
Hemiparesis + UMN Reflexes
Latest
Ipsilateral pupil dilation
Bilateral limb weakness
Irregular breathing
Coma + Death (Respiratory arrest)
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23
Q

What are the main investigation findings in Extradural haemorrhages

A

Biconvex opacity + Midline shift + Brainstem herniation (Poor prognosis) - CT

XR - Skull fracture

NO LP!!!

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24
Q

What are typical triggers of Guillain-Barré syndrome

A

A few weeks after an infection a symmetrical ascending muscle weakness starts.

Triggered after: Campylobacter jejuni, CMV, mycoplasma, Zoster, HIV, EBV, vaccinations.

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25
Q

What is the cause of Guillain-Barré syndrome

A

Due to autoantibodies attacking myelin sheath and schwaan cells.

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26
Q

What are the possible signs and symptoms of Guillain-Barré syndrome

A

Due to autoantibodies attacking myelin sheath and schwaan cells.

Paraesthesia’s in hands and feet frequently precede onset of weakness

Back and leg pain in most cases

Proximal nerves mainly affected - Trunk and respiratory muscles then cranial nerves

Areflexia

Potential autoimmune dysfunction - Sweating, Tachycardia, Arrhythmias, Hypertension

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27
Q

What are the 4 definitive signs of Guillain-Barré syndrome

A

Motor difficulty
Areflexia
Paraesthesia without objective sensory loss
CSF albumin with no cellular reaction

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28
Q

What are the main 4 investigative findings in Guillain-Barré syndrome

A

Slow conduction - Nerve conduction studies
CSF high protein but normal WCC - LP
Monitor FVC every 4 hours and if there is sufficient deterioration mechanically ventilate.

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29
Q

What are the signs of Horner’s syndrome

A 
Unilateral:
Miosis
Ptosis
Anhidrosis
\+ Enopthalmos
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30
Q

Name 3 broad causes of Horner’s syndrome

A

Interruption of faces sympathetic supply at:

The brainstem: Demyelination -MS, Vascular disease - Stroke, Carotid artery dissection

The cord: Syringomyelia

Thoracic outlet: Pancoast tumour

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31
Q

Name 3 potential investigations to investigate Horner’s syndrome

A

Investigating cause:

CXR: Apical lung tumour
CT/MRI: Cerebrovascular accident
CT angio: Dissection

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32
Q

What is the time from diagnosis to death in Huntington’s disease

A

20 years max

It is slow progressing and it is certain death

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33
Q

What are the symptoms seen in the prodromal phase of Huntington’s disease

A

Irritability
Depression
Incoordination

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34
Q

What are the definitive features of late Huntington’s disease

A

Chorea
Dementia
Fits
Death

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35
Q

What part of the brain degenerates in Huntington’s disease

A

Striatum and cortex

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36
Q

What are the main signs and symptoms of Migraines

A 
Potential aura
Throbbing/pulsatile pain
Worsening with movement
Phono/Photophobia
N+V
Usually unilateral
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37
Q

What are common triggers for Migraines

A

CHOCOLATE

Chocolate
Hangovers
Orgasms
Caffeine
Oral contraceptives
Lie-ins
Alcohol
Travel
Exercise
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38
Q

How are Migraines diagnosed

A

Clinically

A least 5 headaches lasting 4-72hrs + N+V/Phono/Photophobia +2 of Unilateral/Pulsating/ Impairs routine activity

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39
Q

What are prophylactic treatments for Migraines

A

BB - Propranolol
Anti-convulsant - Topiramate
TCA - Amitriptyline

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40
Q

What are the treatments for Migraines during attacks

A

Mild
NSAID
Paracetamol
Paracetamol + Aspirin/Caffeine

Severe
Triptans + NSAID
Ergot alkaloids + NSAID
Corticosteroids + NSAID
Butalbital-containing compound + NSAID

All with antiemetics

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41
Q

What are the 4 different Motor neurone diseases

A

ALS - Amyotrophic lateral sclerosis - Motor cortex + Anterior horn = UMN + LMN Signs - Worse prognosis if bulbar onset

Progressive bulbar palsy - CN9-12

Progressive muscular atrophy - Anterior horn = LMN

Primary lateral sclerosis - UMN signs

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42
Q

How can we distinguish between Motor neurone diseases and demyelinating diseases

A

There is no sensory loss or sphincter disturbance in MNDs

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43
Q

How can we distinguish between Motor neurone diseases and Myasthenia Gravis

A

MND never affects eye movements

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44
Q

What are the UMN, LMN and bulbar signs of Motor neurone diseases

A

Typical signs: Spastic gait with foot-drop +/- Proximal myopathy, Weak grip and shoulder abduction or aspiration pneumonia

UMN: Spasticity, Hyper-reflexia, Upgoing plantars

LMN: Wasting, fasciculations

Bulbar: Speech or swelling affected

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45
Q

What is the usual progression of ALS

A

Asymmetrical limb involvement in most cases though it can also start with bulbar signs sometimes or respiratory signs rarely

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46
Q

How would you investigate suspected Motor neurone disease

A

MRI - Structural causes
LP - Inflammatory causes
EMG - Denervation

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47
Q

What is the common diagnostic description for Multiple sclerosis

A

Episodic neurological dysfunction in at least 2 areas of the CNS separated by space and time

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48
Q

What are the most common presentations of Multiple sclerosis

A

Usually monosymptomatic

20% Unilateral optic neuritis (pain on movement and a rapid decline in central vision)

Corticospinal tract and bladder involvement (Autonomic) are common

Foot-drop or spastic paraplegia

Uhthoff’s sign: Symptoms may worsen with heat

Lhermitte’s sign: An electrical sensation that runs down the back and into the limbs when the neck is flexed

Internuclear
Ophthalmoplegia - Lesion in the MLF

49
Q

What are the different types of presentations found in Multiple sclerosis

A

Motor syndromes
Brainstem syndromes
Cerebellar syndromes (ataxia), Sensory syndromes

50
Q

What are investigative findings in Multiple sclerosis

A

Hyper-intensities + demyelinating lesions in the CNS - white matter - MRI
Immunoglobulin bands - CSF PCR

51
Q

What is the cause of Myasthenia Gravis

A

It is caused by autoimmune destruction of postsynaptic NMJ nAChR and the associate proteins (Namely Muscle specific tyrosine kinase)

52
Q

What are the 3 forms of Myasthenia Gravis and what are their associated symptoms

A

Ocular: Ptosis, Diplopia

Oropharyngeal: Dysarthria, Dysphagia, Facial paresis

Generalised: Proximal limb weakness (Worse in evening), Dyspnoea

Generally better with rest and worse with use.

50-60% that present with purely ocular will develop generalised in 1-2 years

53
Q

Which groups of people are usually affected by Myasthenia Gravis

A

<50 Women +/- Rheumatoid Hx +/- Thymic hyperplasia

>50 Men +/- Thymic atrophy/tumour

54
Q

What are the investigative results of Myasthenia Gravis

A
  • Serum AChR antibodies analysis
  • Muscle specific tyrosine kinase (MuSK) antibodies
  • Serial PFTs
55
Q

What are the 3 symptoms defining Parkinsonism

A

Tremor
Hypertonia
Bradykinesia

56
Q

What are the main symptoms of Parkinson’s disease

A

Signs always worse on 1 side.

Parkinsonism+
Sleep disturbance
Anosmia
Autonomic dysfunction (Postural Hypotension, Constipation, Urinary frequency)
Neuropsychiatric dysfunction (Depression, Dementia, Psychosis)

57
Q

How may one investigate atypical Parkinson’s disease

A

Dopaminergic agent trial - Levodopa

58
Q

What is Spinal cord compression

A

Compression of the bloody supply, CSF spaces or cord

59
Q

What are the causes of Spinal cord compression

A

Mainly trauma

Intervertebral disc disease (Herniation)
Vertebral compression - Bone diseases/Steroids
Malignancy
Infection

60
Q

What are the signs and symptoms of Spinal cord compression

A

Sensory (3): Altered sensations, hemisensory loss and pain (Common PC)

Motor (3): Hemi/Para/Tetraplegia or Hemi/Para/Tetraparesis (sparing face)

Autonomic (7): Constipation, Urinary retention, Dizziness, Hypothermia, ED, Abdominal pain, Syncope

61
Q

What are the investigative findings of Spinal cord compression

A

Disc displacement, epidural enhancement mass effect - MRI

Decreased disc space height - XR

Bony fragments + tumour expansion

62
Q

What is Radicuolpathy

A

This is pathology arising from the nerve root

Usually due to mechanical compression

63
Q

What are the cause of Radiculopathy

A

Main causes are intervertebral disc disease and osteoarthritis

Other causes include trauma, Facet joint degeneration, ligamentous hypertrophy, spondylolisthesis

Rare causes include radiation, DM and malignancy

RFs: Obesity, Poor posture, pregnancy

64
Q

What are signs and symptoms of Radiculopathy

A

Sensory (5): Altered sensation, Tingling, Numbness, Shooting pain. Sharp pain (movement)

Motor: Hypo-reflexia, Weakness

65
Q

What are the investigations used in Radiculopathy

A

The same as Spinal cord compression +

EMG - Motor
Nerve conduction studies - Sensory

66
Q

What are the risk factors for Subarachnoid haemorrhage

A 
Smoking
Hypertension
Alcohol
Ehlers-Danlos
Marfans 
Polycystic kidney disease
Neurofibromatosis Type 1
67
Q

What are the signs and symptoms of a Subarachnoid haemorrhage

A

Worst headache of life
Photophobia
LOC
Potential 3rd Nerve Palsy

N&V
Meningism

68
Q

What are the investigative findings in Subarachnoid haemorrhage

A

Hyperdense areas in CT
Xanthochromia in the LP
Troponin I - Elevated

69
Q

What are the cause of Subdural haemorrhage

A

Trauma
Venous
Arteriovenous abnormalities or other systemic bleeding disorders
Anticoagulant use

70
Q

What are the signs and symptoms of a Subdural haemorrhage

A

Headache
N&V
Reduced GCS
Confusion

LOC
Seizure
Incontinence
Neurological changes
Localised weakness
Oto/Rhinorrhoea
71
Q

What are the investigative findings in Subdural haemorrhage

A

Banana shaped mass + Midline shift + Brainstem herniation on CT

XR

No LP

72
Q

Outline the treatment algorithm for Subdural haemorrhage

A

Small <1cm diameter or Midline shift of <5mm:
1st Observational; follow up imaging
+ Prophylactic anti-epileptic (Phenytoin)
A Correction of coagulopathy

Large:
1st Surgery + Everything else

73
Q

What is the most important complication to consider when treating Subdural haemorrhage

A

Epilepsy!! Hence prophylactic anti-epileptics are given

Coma
Neurological defects

Stroke

74
Q

What is the character of Tension headaches

A

Generalised head pain like a tight band around the head with normal neurological examination

Potential
Facial muscle tenderness

75
Q

What is the treatment for Tension headaches

A

Acute - Simple analgesic

Chronic - Antidepressant (Amitriptyline)/Muscle relaxant (Tizanidine)

76
Q

What is the main complication of Tension headaches

A

Peptic ulcer

77
Q

What is the cause of Trigeminal neuralgia

A

80-90% due to nerve compression of 1 or more branches of the trigeminal nerve.

Demyelinating disease - e.g. MS

78
Q

What are the main symptoms of Trigeminal neuralgia

A

Sudden episodes of sharp, stabbing, intense pain lasting up to 2 minutes potentially with a constant component of facial pain.

79
Q

What are common triggers for Trigeminal neuralgia

A

Tooth brushing
Eating
Cold
Touch

80
Q

How is Trigeminal neuralgia diagnosed

A

It is a clinical diagnosis but one may perform:
Trigeminal reflex testing
MRI or
Intraoral XR

81
Q

Who is more susceptible to Wernicke’s encephalopathy

A

It is caused by a deficiency in thiamine leading to focal areas of brain damage

Chronic Alcoholism
Eating disorders
Malnutrition
Prolonged vomiting (e.g. Chemo, GI malignancy, Hyperemesis gravidarum)
AIDS
Thyrotoxicosis
82
Q

What are the signs and symptoms of Wernicke’s encephalopathy

A

Triad:
Confusion
Ataxia
Ophthalmoplegia (Nystagmus, Lateral rectus or conjugate gaze palsies)

Memory disturbances
Hypotension
Hypothermia
Reduced consciousness
Hallucinations

Korsakoff’s psychosis = Deterioration leading to:
Amnesia &
Confabulation

83
Q

How is Wernicke’s encephalopathy diagnosed

A

Diagnosis is mainly based on history and examination

Therapeutic trial of parenteral thiamine - Clinical response

Blood alcohol level
Blood thiamine and its metabolites

84
Q

What is the normal ICP in adults

A

<15mmHg

85
Q

What are causes of Raised ICP

A 
Tumour
Haemorrhage
Hydrocephalus
Cerebral oedema
Head injury
Infection: Meningitis, encephalitis, brain abscess
Status epilepticus
86
Q

What are the signs and symptoms of Raised ICP

A

Headaches (Worse on coughing, leaning forward)
Vomiting
Altered GCS
Cushings response: Bradycardia, hypertension and irregular breathing (Cheyne-Stokes)
Pupil changes - Constriction then later dilation
Decreased visual acuity, peripheral field loss
Papilloedema is an unreliable sign - Venous pulsation at the disc may be absent

87
Q

What are the appropriate investigations for Raised ICP

A

U&Es, FBC, LFT, Glucose, Serum osmolality, clotting, blood culture.

Toxicology screen

CXR - Any source of infection?

CT head

LP if safe (Measure the opening pressure)

88
Q

What is Neurofibromatosis

A

This is an autosomal dominant genetic disorder affecting cells of neural crest origin resulting in the development of multiple neurocutaneous tumours

89
Q

What the different classifications of Neurofibromatosis and what are the definitive features of each

A 
Type 1 (von Recklinghausen's disease):
Peripheral and spinal neurofibromas
Multiple cafe au lait spots
Freckling axillary/inguinal
Optic nerve glioma
Lisch nodules
Skeletal deformities
Phaechromocytomas
Renal artery stenosis
Type 2:
Schwannomas
Meningiomas
Gliomas
Cataracts
90
Q

What are the presenting symptoms of Neurofibromatosis

A

FHx

Type 1:
Skin lesions
Learning difficulties
Headaches
Disturbed vision (due to optic gliomas)
Precocious puberty
Type 2: 
Hearing loss - Sensorineural
Tinnitus
Balance problems
Headache
Facial pain
Facial numbness
91
Q

What are the appropriate investigations for Neurofibromatosis

A 
Ophthalmological assessment
Audiometry
MRI for tumours
Skull XR - Sphenoid dysplasia in NF1
Genetic testing NF TSG Mutations
92
Q

What is hydrocephalus and how can it be classified

A

It is enlargement of the ventricular system

Obstructive (Non-communicating) or Non-obstructive (Communicating)

There is also hydrocephalus ex vacuo = Apparent enlargement of the ventricles as a compensatory change due to brain atrophy

93
Q

What are obstructive and non-obstructive causes of CSF accumulation

A

Obstructive: Impaired outflow:
Lesion of 3rd or 4th ventricle or cerebral aqueduct
Posterior fossa lesions compressing the 4th ventricle
Cerebral aqueduc stenosis

Non-obstructive: Impaired CSF reabsorption into subarachnoid villi:
Tumour
Meningitis
Normal pressure hydrocephalus - Idiopathic - White matter tracts destroyed

94
Q

Who is likely to suffer from Hydrocephalus

A

Biomodal
Young - Congenital malformations and brain tumours
Elderly - Strokes and tumour

95
Q

What are the signs and symptoms of Hydrocephalus

A

Obstructive: Acute drop in conscious level - Low GCS
Diplopia - 6th Nerve palsy
Papilloedema
Neonates: Increased head circumference + Sunset sign (Downward conjugate deviation of the eyes)

Normal pressure: Triad:
Dementia
Gait disturbance
Urinary incontinence
Hyper-reflexia
96
Q

What are the investigative signs of Hydrocephalus

A

Ventricular enlargement - CT
CSF from ventricular drainage may indicate pathology
LP contraindicated if raised ICP but therapeutic for normal pressure hydrocephalus

97
Q

What are the causes of Transient ischaemic attacks

A

Usually embolic but may be thrombotic - Usually from a carotid atherosclerosis

Emboli can also arise from the heart due to AF, Mitral valve disease or Atrial myxoma

Clots from the right side can cause stroke if there is a septal defect

RFs: HTN, DM, HD, Hyperlipidaemia, Alcohol, Smoking, Peripheral artery disease, Polycythaemia ruby vera, COCP, Clotting disorders

98
Q

What are the typical history of a Transient ischaemic attack

A

Brief duration of symptoms + Report of neurological defect

Unilateral symptoms
Increased BP on presentation
Focal neurological deficit on examination
No positive symptoms
No headache
No epilepsy
Hx Migraine
Hx Cardiac disease

Carotid Bruit

99
Q

What are the investigative findings in Transient ischaemic attacks

A 
Potential
Blood glucose - Hypo
Coag - Coagulopathy
ECG - AF
MRI/CT Head- Half will have positive diffuse images
Echo
100
Q

How is Transient ischaemic attack treated?

A

Atherosclerotic / Small-vessel
1st - Antiplatelet = Aspirin, Clopidogrel
+ Antihypertensive
+ >50% Carotid stenosis - Endarterectomy or stent

Cardioembolic no IHD
1st - Anticoagulant = Warfarinf/Noax
2nd - Antiplatelet + Statin

Cardioembolic + IHD
1st - Anticoagulant + Statin

101
Q

What are the 2 main types of seizure

A

Focal: Specific cortical regions (Complex/Simple)
Generalised: Affect the whole brain affecting consciousness

102
Q

What are the 5 main types of generalised seizure

A 
Tonic-Clonic
Myotonic
Absence
Atonic
Tonic
103
Q

What are the causes of Epilepsy?

A 
Most idiopathic
Cerebrovascular disease
Head injury
Cranial surgery
CNS infections 
Neurodegenerative
Autoimmune diseases
Tumour
Drugs
Metabolic: Uraemia, Hypoglycaemia, Hypo/Hypernatraemia, Hypo/Hypercalcaemia
104
Q

What are the presentations of Epilepsy

A

Generalised seizures cause disturbance in consciousness. Tonic, Clonic, Postictal phases.

Seizures associated with tongue biting and incontinence.

In the postictal phase there is often headache and drowsiness. Amnesia both the event and circumstance

Absence - Interruption to mental activity for less than 30 seconds

Focal - Aura, focal motor activity during seizure, automatisms

105
Q

What investigations are performed in Epilepsy

A

EEG - Confirm diagnosis, classify

CT/MRI - Shows structural, space-occupying or vascular lesions

106
Q

How is Epilepsy treated

A

Focal - Carbamazepine or lamotrigine
Generalised - Sodium Valproate
Status epilepticus - Diazepam

+ Patient education

107
Q

What are complications of Epilepsy

A

Fractures
Behavioural problems
Sudden death in epilepsy
Neutropenia + Osteopenia - Carbomazepine

108
Q

What are the main causative organisms in Meningitis

A

Meningococcus or pneumococcus.

Less commonly Haemophilus influenzae; Listeria or TB if immunocompromised eg HIV +ve, organ transplant, malignancy

Viral: HSV, VZV, enteroviruses. CMV,

Fungal: Cryptococcus

109
Q

What are risk factors for Meningitis

A 
Crowded space
Basal skull fractures
Mastioditis
Sinusitis
Inner ear infections
Alcoholism
Immunodeficiency
Splenectomy
Sickle cell anaemia
CSF shunts
Intracranial surgery
110
Q

What are the signs and symptoms of Meningitis

A

Early: Headache, Fever

Later:
Photophobia
Neck stiffness
Irritability
Drowsiness
Vomiting
Lowering GCS

Travel and exposure history!

Signs
Kernig's sign
Brudzinski's sign
Skin rash - Non-blanching
Hypotension
Tachycardia
Altered mental status
111
Q

What are appropriate investigations in Meningitis

A

CSF:
Bacterial - Turbid, PMN, Low Glucose, Higher Protein
TB - Fibrin web, Lympho, Low Glucose, Highest Protein
Virus - Clear, Lympho, High Glucose, High Protein

112
Q

How is Meningitis treated

A

IV Antibiotics - Ceftriaxone, Amoxicillin
Dex IV
Airway support
Fluid restriction

113
Q

What are the possible complications associated with Meningitis

A 
Septicaemia
Shock
DIC
Renal failure
Seizures
Raised ICP
114
Q

Outline the aetiology of Stroke

A 
Ischaemic (80%):
Thrombosis
- Small vessel - Lacunar
- Large vessel
- Prothrombic state (Dehydration, thrombophilia)

Emboli
- Carotid dissection/athersclerosis, AF

Hypertension
- Watershed zones infarct when blood pressure is below auto regulatory range

Vasculitis/Cocaine

Haemorrhagic (20%):

  • Hypertension
  • Microaneurysm
  • Amyloid antipathy
  • Arteriovenous malformations
115
Q

What are the different presentations of Stroke based on location

A

Anterior circulation: Anterior cerebral artery

  • Contralateral Hemiparesis - Legs more than arms
  • Confusion
  • Executive function disturbances

Anterior circulation: Middle cerebral artery

  • Facial weakness
  • Contralateral Hemiparesis - Arms more than legs
  • Contralateral Hemisensory loss
  • Hemianopia
  • Aphasia if left sided

Posterior Circulation: Posterior cerebral:

  • Homonymous Hemianopia
  • Visual agnosia

Anterior inferior cerebellar
- Vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness

Posterior inferior cerebellar
- Vertigo, ipsilateral ataxia, ipsilateral Horner’s syndrome, ipsilateral hemisensory loss, dysarthria, contralateral spinothalamic sensory loss

116
Q

How is a stroke diagnosed

A

Non-contrast CT head within 25 mins - Excludes haemorrhage

MRI after if available

ECG - Check for arrhythmia
Echo - Cardiac thrombus
CT Angio - Detect dissections or intracranial stenosis
Carotid doppler - Check carotid artery disease

Bloods - Glucose, U&Es, Cardiac enzymes

117
Q

How is stroke treated

A

<4.5 Hrs with no contraindications to thrombolysis:

1st Line - Alteplase 0.9mg/Kg (10% as bolus with remaining 90% as infusion over 1hr) Max 90mg
A - Aspirin 24hrs after Alteplase 300mg
+ Supportive (O2, Glucose, BP, Fever)
+ Swallowing assessment
A - Prophylactic VTE and early mobilisation (Heparin/LMWH)

> 4.5 Hrs with no contraindications to thrombolysis:
1st Line: Aspirin 300mg
+ Supportive
+ Swallowing assessment
A - Prophylactic VTE and early mobilisation (Heparin/LMWH)

Cerebral venous sinus thrombosis:
- Anticoagulation (Heparin/Warfarin)
+ Supportive
+ Swallowing assessment

Contraindications to thrombolysis include:

  • Negative CT head
  • Head trauma
  • MI
  • GI or UG Haemorrhage
  • Recent surgery
  • Hx IC Haemorrhage
118
Q

What are complications of Stroke

A 
Cerebral oedema
Immobility
Infections
DVT
Cardiovascular events
Death
119
Q

What are the different types of MS

A

Relapsing-remitting - Most common - Clinical attacks of demyelination with complete recovery

Clinically isolated syndrome - Single clinical attack of demyelination 10-50% progress to MS

Primary progressive MS - Steady accumulation of disability with no relapsing-remitting pattern

Marburg Variant - Severe variant of MS leading to advanced disability or death within weeks

All conditions - Year 3 (16 decks)

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