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Medical Diseases > Neurology disease summaries > Flashcards

Neurology disease summaries Flashcards

1
Q

Stroke

A

Rapidly developing clinical symptoms and/or signs of focal, and at times global, loss of brain function, with symptoms lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin

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2
Q

CVA types

A

Infraction/Ischaemia

  • thrombus formation or embolus (cardioembolic/thromboembolic)
  • atherosclerosis
  • shock
  • vasculitis

Intracranial haemorrhage

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3
Q

CVA risk factors

A 
CVD: angina, MI or PVD
Previous stroke or TIA
Atrial fibrillation
Carotid artery disease
Atheroma 
Hypertension
Diabetes and Smoking
Vasculitis
Thrombophilia
Combined contraceptive pill
Age > 70 years/Male
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4
Q

stroke symptoms

A
  1. Sudden weakness of limbs: initially flaccid and then spastic (UMN)
  2. Sudden facial weakness
  3. Sudden onset dysphasia (speech disturbance)
  4. Sudden onset visual or sensory loss e.g. homonymous hemianopia
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5
Q

TACS

A
  1. Unilateral weakness (and sensory deficit) of face, arm and leg
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorders)

Emboli

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6
Q

PACS

A

Two of the following:

  1. Unilateral weakness (and sensory deficit) of face, arm and leg
  2. Homonymous hemianopia
  3. Higher cerebral dysfunction e.g. dysphasia, visuospatial disorders)
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7
Q

LACS

A

One:

Pure sensory
Pure motor
sensori-motor
ataxic hemiparesis

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8
Q

POCS

A

One:

CN palsy and contralateral motor/sensory deficit

bilateral motor/sensory deficit

conjugate eye movements

cerebellar dysfunction e.g. ataxia, nystagmus

isolated homonymous hemianopia or cortical blindness

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9
Q

Stroke management

A

CT (diffusion weighted MRI - bleed or infarct)

No bleeding - aspirin 300mg STAT and then for 2 weeks

Thrombolysis with alteplase within 4.5 hours

Endarterectomy - within 6 hours

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10
Q

Stroke - secondary management

A

mild stroke: aspirin 300mg stat, 2 weeks of 300mg) and clopidogrel for up to 3 weeks. Then step down to clopidogrel 75mg OD

Atorvastatin 80mg

If AF

  • Heparin
  • Intermittent pneumatic compressions

reduce BP gradually

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11
Q

TIA

A

Defined as transient neurological dysfunction secondary to ischaemia (lack of blood flow) without infarction (death of tissues).

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12
Q

TIA management

A
  1. Aspirin 300mg daily
  2. clopidogrel
  3. Carotid endarterectomy
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13
Q

Receptive dysphagia

A

is difficulty in comprehension: Wernickes area (superior temporal)

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14
Q

Expressive dysphagia

A

difficulty in putting words together to make meaning: Broca Area (frontal)

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15
Q

intracranial bleeds signs/symptoms

A

Seizures

Focal weakness

Vomiting

Reduced consciousness`

Other sudden onset neurological symptoms

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16
Q

GCS

A 
Eyes
	Spontaneous = 4
	Speech = 3
	Pain = 2
	None = 1
Verbal response
	Orientated = 5
	Confused conversation = 4
	Inappropriate words = 3
	Incomprehensible sounds = 2
	None = 1

Motor response
 Obeys commands = 6
 Localises pain = 5
 Normal flexion = 4
 Abnormal flexion = 3 (Decorticate posturing)
 Abnormal Extension = 2 (decerebrate posturing)
 None = 1

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17
Q

Decorticate posturing

A

lateral corticospinal tracts are disrupted so the rubrospinal tracts takes over causing the abnormal flexion to the upper extremities and the reticulospinal tracts takes over causing the extension of the legs.

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18
Q

Decerebrate

A

Below the red nucleus

In this case, both the lateral cortical spinal tract and rubrospinal tract are damage so the reticulospinal tract takes over and causes extension of the whole body.

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19
Q

Subdural haematoma

A

collection of blood between the dura and the arachnoid layer, typically caused by a traumatic event.

damages bridging veins (drain cortex and into sinuses)

elderly, alcoholics and epileptics

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20
Q

Acute SDH SIGNS/SYMPTOMS

A

decreased state of consciousness
Headache
personality change and unsteadiness

Raised ICP, seizures, localising neurological symptoms. unequal pupils, hemiparesis) occur late up to 1 month after injury

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21
Q

SDH diagnosis

A

CT scan they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).

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22
Q

chronic SDH

A

brain ages - bridging veins are stretched and even minor trauma can rupture. Longer course (3-7 weeks)

leaky vessels result in the accumulation of blood in the subdural space and an osmotic gradient can form which draws more fluid in that space.

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23
Q

chronic SHD signs/symptoms and diagnosis

A

mean of 3-7 weeks before symptoms starts to present.

The most common presenting complaints are headache and confusion. Other symptoms include: urinary incontinence, weakness, seizures, cognitive dysfunctions and gait abnormalities

hypodense on CT scan

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24
Q

SDH management

A

prevent secondary insults

  1. hypoxia, hypotension and mass lesions
  2. control ICP and CPP

Craniotomy or burr hole washout

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25
Q

Raised ICP medical management and surgical

A

Sedation: Propofol, benzodiazepines, barbiturates

Maximise venous drainage of brain

  • Head of bed tilt: 30 degrees for head position
  • Cervical collars, ET tube ties

CO2 control

Osmotic diuretics (Mannitol, Hypertonic saline)

CSF release

surgical: decompressive craniectomy

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26
Q

EDH

A

rupture of the middle meningeal artery (the anterior branch of the middle meningeal artery is vulnerable to injury as it runs underneath the pterion) in the temporo-parietal region.

associated with a temporal fracture

between skull and dura

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27
Q

EDH signs/symptoms

A

brief loss of consciousness, followed by a period in which the patient regains consciousness and awareness (called a lucid interval: can be a few hours to a few days)

After that the patients further deteriorates, exhibiting symptoms such as: headache, vomiting, contralateral hemiparesis with brief reflexes

If bleeding continues, the ipsilateral pupillary dilatation (causes the uncus of the temporal lobe to herniate and compress on the pupillary fibres of the oculomotor nerve).

Bilateral weakness develops and breathing becomes deep and irregular (brainstem compression)

Death follows a period of coma

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28
Q

EDH diagnosis

A

CT scan they have a bi-convex shape and are limited by the cranial sutures

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29
Q

Intracerebral haemorrhage Iv

A

CT scan: Well demarcated intra-parenchymal haematomas

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30
Q

Intracerebral haemorrhage management

A

• Surgical evacuation of haematoma +/-treatment of underlying abnormality

Good - if small superficial clot and good neurological status

Poor - if large basal ganglia or thalamic clot with major focal deficit or deep coma

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31
Q

Subarachnoid Haemorrhage

A

bleeding into the subarachnoid space, where the cerebrospinal fluid is located. Between pia and arachnoid membrane

Usually an aneurysm

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32
Q

Subarachnoid Haemorrhage signs/symptoms

A

sudden onset occipital headache that occurs during strenuous activity “thunderclap headache”

N&V, neck stiffness and photophobia (meningeal irritation), Kernigs sign, focal neurological changes, 3rd nerve palsy (posterior communicating artery aneurysm)

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33
Q

Subarachnoid Haemorrhage Iv

A

CT
LP
Angiography (CT or MRI)

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34
Q

Subarachnoid Haemorrhage management

A

surgical: coiling or clipping

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35
Q

Subarachnoid Haemorrhage complications

A

vasospasm: prolonged arterial contraction - delayed ischaemic neurological deficit (3-14 days)
- nimodipine

rebleeding

SIADH: hyponatraemia

Hydrocephalus

antiepileptic medications

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36
Q

Arteriovenous malformations

A

AVM is a complex tangle, or nidus, of arteries and veins connected together with one or more fistulas, creating a shunt (no capillary bed present).

Usually intraparenchymal

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37
Q

Arteriovenous malformations Iv and management

A

Catheter angiography

If accessible to surgery then an open craniotomy is done with excision of AVM

Stereotactic radiosurgery: if risk of surgery outweighs the benefit. This procedure is accepted for some small AVMs and/or deep AVMs
AVM is in eloquent brain/deep tissue inaccessible to surgery then endovascular coiling can be considered

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38
Q

Cavernous malformation

A

well circumscribed benign vascular lesions encompassing sinusoidal spaces lined by endothelium and separated by elastin (gross pathology resembles a mulberry), with a rim of hemosiderin-laden macrophages surrounding it.

No intervening brain parenchyma

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39
Q

Cavernous malformation Ix

A

CT

MRI: popcorn

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40
Q

Dural venous sinus thrombosis - most common

A

sagittal sinus thrombosis or transverse sinus thrombosis

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41
Q

Cortical sinus thrombosis

A

Usually occurs with a sinus thrombus as it extends into the cortical veins causing infarction in venous territory.

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42
Q

Multiple sclerosis

A

Chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system.

young adults and women

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43
Q

MS causes

A

Multiple genes, Epstein–Barr virus (EBV), Low vitamin D, Smoking, obesity, living near the equator

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44
Q

Pyramidal dysfunction

A

Increased tone

spasticity: velocity dependent increase in tone
- extensors: upper limb
- flexors: lower limb

Weakness:

  • upper limbs: flexors strong, extensors weak
  • lower limbs: extensors strong, flexors weak
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45
Q

MS signs/symptoms

A 
Pyramidal dysfunction
Optic neuritis 
Sensory symptoms 
LUTD
Cerebellar 
Fatigue 
Cognitive impairment
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46
Q

Optic neuritis

A

demyelination of the optic nerve and unilateral loss of vision

  • central scotoma
  • pain on eye movement
  • impaired colour vision (dyschromatopsia)
  • RAPD
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47
Q

MS: Disease patterns

A

Clinically isolated syndrome

relapsing/remitting

Secondary progressive

Primary progressive

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48
Q

MS Iv

A

over 1 year
2 episodes suggestive of demyelination and dissemination in time and place
LP: oligoclonal bands in CSF

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49
Q

Acute exacerbation/relapse MS treatment

A

Mild: symptomatic treatment or observe and it gets better
- amitriptyline or gabapentin for paranaesthesia/neuralgia/neuropathic pain

Moderate – oral steroids e.g. methylprednisolone for 5 days

Severe – admit/IV steroids (1g IV daily for 3-5 days)

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50
Q

Optic neuritis acute management

A

IV methylprednisolone followed by oral prednisolone

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51
Q

Pyramidal dysfunction management (MS)

A
  • Exercises
  • Oral baclofen and Tizanidine
  • Benzodiazepine
  • B toxin in joints
  • intrathecal baclofen/phenol
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52
Q

Sensory symptoms (MS) treatment

A

Anti-convulsant e.g. gabapentin

Anti-depressant e.g. amitriptyline

Tens machine

Acupuncture

Lignocaine infusion

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53
Q

LUTD management (MS)

A

Bladder drill (training)

Anti-cholinergic e.g. oxybutynin and tolterodine (worsen cognitive impairment)

Desmopressin e.g. long journey

Catheterisation e.g. significant retention

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54
Q

Disease modifying MS

A

1st line therapy: relapsing and remitting

  • Tecfidera, aubagio
  • Interferon Beta – injection (sc/IM):
  • Glitiramer Acetate -injection

2nd therapy: RRMS

  • Anti CD20 (ocrelizumab, Rituximab)
  • Anti CD 50 (Alemtuzemab)
  • Anti integrin (Natilizumab)
  • Fingolimod, cladrabine

3rd line:

  • Mitoxantrone
  • HSCT
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55
Q

Motor Neurone disease

A

Progressive, ultimately fatal condition where the motor neurones stop functioning (motor neuron degeneration/death)

Selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells

no effect on the sensory neurones or sphincter disturbance and patients should not experience any sensory symptoms.

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56
Q

MND types

A
  1. Amylotropic lateral sclerosis: UMN/LMN: Motor cortex and anterior horn cells
  2. Progressive bulbar palsy: CNIX-XII, UMN/LMN
  3. Primary lateral sclerosis: UMN - loss of betz cells in motor cortex
  4. Progressive muscular atrophy - LMN - loss of anterior horn cells
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57
Q

MND signs/symptoms

A

late middle aged (e.g. 60) man, possibly with an affected relative spastic gait, foot drop +/- proximal myopathy, weak grip and shoulder abduction

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58
Q

LMN signs/symptoms

A

o Muscle wasting
o Reduced tone
o Fasciculations (twitches in the muscles)
o Reduced reflexes

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59
Q

UMN signs/symptoms

A 
o	Increased tone or spasticity
o	Brisk reflexes/hyperreflexia 
o	Upgoing plantar responses
o	Spastic gait 
o	Exaggerated jaw jerk 
o	Slowed movements
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60
Q

Bulbar variant (Motor Neurone) management

A

Communication needs (Speech therapy, technology from tablets to ‘voice banking’, pen and paper when tired)

small high energy supplements

early insertion of gastrostomy tubes (PEG, RIG or NG tube)

sialorrhoea

  • hyoscine/buscopan
  • Glycopyrronium
  • botox
  • suction
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61
Q

Riluzole

A

the progression of the disease and extend survival by a few months in AML. causing lots of liver and kidney problems (needing blood tests) and only gives you 3 months of disabling
inhibitor of glutamate and NMDA receptor antagonist

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62
Q

Parkinson’s Disease

A

progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement (hypokinetic)

Loss of dopaminergic neurons from the pars compacta region of the substantia nigra and the presence of alpha-synuclein containing inclusions known as Lewy bodies in specific areas of the brain

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63
Q

Parkinson’s Disease risk factors

A 
Age – most important 
Male sex – slight increase 
Rural living – slight increase 
Smoking – decreases risk 
FH of Parkinson’s disease
Drugs - cyclizine or metaproclomide
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64
Q

Parkinson’s Disease signs/symptoms

A

PD: usually asymmetrical

  1. Resting tremor (improves with movement)
  2. Rigidity: Cogwheel
  3. Bradykinesia (slower movements)
  4. Postural disturbances
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65
Q

Other signs/symptoms of PD

A 
Depression
Sleep disturbance and insomnia (lack of REM sleep?)
Loss of the sense of smell (anosmia)
Cognitive impairment and memory problems
GI dysfunction
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66
Q

PD should not present with

A

Postural instability leading to falls occurs relatively late in the clinical course of PD (if it is happening early, back to differential diagnosis)

Failure to respond to even large doses of levodopa is usually a strong indicator that the patient does not have idiopathic PD

Early-onset bulbar problems, dementia and hallucinations, preferential involvement of lower limbs

Prominent eye movement disorder (*supranuclear eye palsy)

Intrusive early autonomic problems

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67
Q

PD management

A
  1. levodopa: cross BBB
    - combined with peripheral decarboxylase inhibitors e.g. carbidopa/co-careldopa
    - reserved when other treatments become ineffective and symptoms less controlled
  2. COMT inhibitors e.g. entacapone
    - take with levodopa in brain
  3. Dopamine agonist e.g. bromocrytine.
    - delay the use of levodopa in early disease and are then used in combination with levodopa to reduce the dose of levodopa
    - apomorphine (continuous sc infusion)
  4. Monoamine oxidase-B-inhibitors e.g. selegiline: specific to dopamine, help increase circulating dopamine
  5. Anticholinergics such as trihexyphenidyl or diphenhydramine (Benadryl) aim to combat tremor, but usually cause severe side effects
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68
Q

PD side effects of medication

A
  1. dopamine side effects
    - dystonia
    - chorea
    - athetosis
    - Vomiting: doperidone
  2. dopamine agonists
    - pulmonary fibrosis
    - daytime somnolence & oedema
  3. Impulse control disorders, including pathological gambling, hypersexuality, binge eating, compulsive spending occur much more often with dopamine agonists
  4. Hallucinations and not prescribed in elderly with CI
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69
Q

Drug induced psychosis PD Mx

A

clozapine (agranulocytosis) and quetiapine

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70
Q

Vascular Parkinsonism

A

clinical features of parkinsonism that are presumably caused by cerebrovascular disease

  • predominantly lower limbs (lower body parkinsonism)
  • rest tremor uncommon
  • spasticity, hemiparesis and pseudobulbar palsy
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71
Q

Vascular Park Iv

A

Poor levodopa response

Structural brain imaging will guide diagnosis

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72
Q

Drug Induced Parkinsonism Mechanism

A

Medicines: block the action of dopamine, the neurotransmitter that is gradually lost in the brains of people with Parkinson’s. They include: Neuroleptic or antipsychotic drugs used to treat schizophrenia and other psychiatric problems.

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73
Q

Drug Induced parkinsonism signs/symptoms

A
  1. Symmetrical
  2. Postural Tremor e.g. oustretched arms
  3. Orolingual dyskinesias, tardive dystonia and akathisia
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74
Q

Drug induced parkinsonism mx

A

remove drug that blocks dopamine

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75
Q

benign essential tremor

A

AD, fine tremor of voluntary muscles

  • Fine tremor (Hands the most however can affect head, jaw and vocal)
  • Symmetric, postural or kinetic tremor with higher frequency (up to 12 Hz)
  • more prominent on voluntary movement
  • Worse when tired, stressed or after caffeine
  • Alcohol responsiveness: improved
  • Head tremor – if present – mild
  • Absent during sleep (no voluntary movements during sleep)
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76
Q

Benign essential tremor mx

A

to improve symptoms

  1. propranolol
  2. Primidone
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77
Q

Multi system atrophy

A

neurones of multiple systems of nerves in the brain to degenerate including basal ganglia

6th and 7th decade

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78
Q

Multi-system atrophy signs/symptoms

A

autonomic dysfunction (postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (ataxia)

core triad: dysautonomia, cerebellar features and parkinsonism

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79
Q

Progressive supranuclear palsy

A

Symmetric akinetic-rigid syndrome with predominantly axial involvement. PSP occurs when brain cells in certain parts of the brain are damaged as a result of a build-up of a protein called tau.

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80
Q

Primary dementias

A

AZ, Picks, Lewy body, Huntington’s

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81
Q

Alzheimer disease

A

Neurodegenerative proteinopathy (amyloid)

usually sporadic
Familial: APP (amyloid precursor), presenilin 1 & 2 and e4

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82
Q

Pathology of AD

A

Disruption of cholinergic pathways in the brain + synaptic loss: Loss of cortical neurones (decrease in front, temporal and parietal lobe atrophy)

  • neurofibrillary tangles (tau)
  • senile plaques of amyloid b protein (extracellular)
  • both cause excitotoxicity
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83
Q

AD Ix

A

clinical
MRI: temporal and parietal loss
SPECT: temporoparietal and reduced metabolism
CSF: Reduces amyloid and increase in tau

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84
Q

AD Mx

A

Cholinesterase inhibitors - rivastigmine, galantamine and donepezil

NMDA receptor blocker e.g. Menantine - protects against too much glutamate

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85
Q

Dementia with lewy bodies

A

Protein deposits called Lewy bodies, develop in nerve cells in the brain regions involved in thinking, memory and movement (motor control).

Neurodegenerative proteinopathy (a-synuclein)

late onset dementia > 65 years

Leads to disruption of cholinergic (memory problems) and dopaminergic pathways (PD features)

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86
Q

signs/symptoms of lewy body

A

progressive cognitive decline but is fluctuating cognitive impairment

There are associated symptoms of visual hallucinations (shadow behind them or animals/faces at the window), delusions, disorders of REM sleep and fluctuating consciousness

Motor features of parkinsonisms

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87
Q

Lewy Body Ix and Mx

A

Dat and alpha synuclein ligand imaging/a-synuclein in CSF

Mx

  • small levodopa dose
  • trial cholinesterase inhibitors
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88
Q

Parkinsons disease dementia

A

PDD >1 year of presentation

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89
Q

Huntington’s chorea

A

AD “trinucleotide repeat disorder” that involves a genetic mutation in the HTT gene on chromosome 4. Production of abnormal glutamine residues (toxic)

Anticipation: earlier age of onset and increased severity

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90
Q

Huntington’s chorea pathology

A

loss of basal ganglia cells (basal ganglia, cuada and putamen) and cortex (frontal, parietal)

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91
Q

HC signs/symptoms

A
  1. 30-50 yrs
  2. cognitive, psychiatric or mood problems
  3. development of movement disorders
    - Chorea (involuntary, abnormal movements)
    - Rigidity and inability to walk
    - Bradykinesia
    - Eye movement disorders
    - dysarthria
    - dysphagia
    - Myoclonus
    - slurred speech, depression , irritability and apathy
    - eventual involvement of memory
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92
Q

HD Mx

A

MDT
Mx for disordered movement
- Antipsychotics (e.g. olanzapine)
- Benzodiazepines (e.g. diazepam)
- Dopamine-depleting agents (e.g. tetrabenazine): Huntington’s: too much dopamine therefore lose it
- Depression can be treated with antidepressants.

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93
Q

Picks

A

dementia commencing in middle life (usually between 50 and 60 years) characterised by progressive changes in character and social deterioration leading on to impairment of intellect, memory and language

Build up of Tau

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94
Q

Picks signs/symptoms

A

Personality and behavioural change (apathy [lack of interest], loss of empathy, stereotyped or compulsive behaviours, hyperorality)
Find it very difficult to stop behaviours when they start (compulsive behaviour)
Speech and communication problems
Change in eating habits
Reduced attention span

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95
Q

Picks Ix and Mx

A

MRI: focal atrophy of frontotemporal lobes

SPECT: frontotemporal reduced metabolism

CSF: increased tau/normal amyloid (not affected in this)

Mx
- Trazadone: anti-depressant/anti-psychotic - slightyl sedative

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96
Q

Vascular dementia

A

sudden onset and stepwise deterioration

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97
Q

Multi infarct dementia

A

Disorder involving a deterioration in mental function due to cumulative damage to the brain through hypoxia or anoxia (lack of oxygen) as a result of multiple blood clots within the blood vessels supplying the brain

Successive multiple cerebral infarctions cause increasingly larger areas of cell death and damage

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98
Q

Multi-infarct dementia Ix

A

aware of it
Abrupt onset
Stepwise progression (further small infarcts occurring)
history of hypertension or stroke
Evidence of stroke will be seen on CT or MRI

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99
Q

Functional Cognitive impairment

A

everyday forgetfulness
Scores well at congitive tests such as addenbrookes test and still does a hard job

Mx
Exclude a mood disorder (depression can cause deficits in attention, excutive function and memory)

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100
Q

Prion disease

A

Most common human prion disease = Creutzfeldt-jakob disease

Natually occuring PrPc (everyone has it) – misfolded PrPsc = neurodegeneration

Most concentrated in CNS and lymphatics

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101
Q

Prion disease types

A
  • sporadic
  • variant: Bovine spongiform encephalopathy
  • iatrogenic
  • genetic
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102
Q

Transient global amnesia

A
  • sudden, temporary episode of memory loss that can’t be attributed to a more common neurological condition, such as epilepsy or stroke
  • transient changes in the hippocampus in temporal lobe (where memories are stored)
  • anterograde > retrograde amnesia
  • transient 4-6 hours
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103
Q

Transient epileptic amnesia

A

Transient epileptic amnesia (TEA) is a rare but probably underdiagnosed neurological condition which manifests as relatively brief and generally recurring episodes of amnesia caused by underlying temporal lobe epilepsy.

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104
Q

Transient epileptic amnesia

A

complex activities with no recollection events

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105
Q

Meningitis causes with ages (bacteria)

A
  • Neonates – group B streptococcus (GBS) & Listeria – Contracted at birth in mother’s vagina
  • Ages 10-21: Neisseria meningitidis: meningococcus
  • Age over 21: Streptococcus pneumoniae (pneucmococcus)
  • Over 65 : Streptococcus pneumoniae > Listeria
  • Immunosuppressed & Alcoholics: listeria monocytogenes and haemophilus influenza
  • Neurosurgery/ head trauma: Staphylococcus, Gram negative bacilli
  • Fracture of the cribiform plate: Streptococcus pneumoniae
106
Q

Viral meningitis types

A

HSV, VZV and enterovirus

107
Q

Meningitis signs/symptoms

A

Fever, neck stiffness, vomiting, headache, photophobia, lethargy, confusion altered consciousness and focal signs such as seizures

Meningococcal septicaemia: classic petechial rash “non-blanching rash”
disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages

108
Q

Meningitis Ix

A 
Kernig's test 
Brudzinskis test 
Blood cultures
Throat swab 
Blood EDTA PCR
CSF LP
109
Q

Meningitis Mx

A

IM Benzylpenicillin

  1. Ceftriazone IV 2g + Dexamethasone IV 10mg qds 7 + amox (if listeria is suspected)
    - pen allergic (chloramphenicol)
    - pen allergic and listeria (co-trimoxazole IV)
    - Vancomycin - if pen resistant
110
Q

Prophylaxis Meningitis Mx

A

Ciprofloxacin 500mg

111
Q

aspectic meningitis

A

non-pyogenic bacterial meningitis
o A low number of WBC
o A minimally elevated protein
o A normal glucose

112
Q

Encephalitis

A

inflammation of brain

- commonly viral, HSV1/2, VZV (chickenpox), cytomegalovirus (immunodeficiency), EBV

113
Q

Encephalitis signs/symptoms

A 
Cerebral cortex is diffusely involved 
Altered consciousness/stupor/coma
Altered cognition
•	Confusion/psychosis 
•	Unusual behaviour and speech disturbances
•	Acute onset of focal neurological symptoms e.g. seizures and partial paralysis 
•	Acute onset of focal seizures
•	Fever
114
Q

Encephalitis Mx

A

If delay start pre-emptive aciclovir as prompt therapy improves outcomes [death]

Aciclovir treats herpes simplex virus (HSV) and varicella zoster virus (VZV)
o Ganciclovir treat cytomegalovirus (CMV)
o Treat with antibiotics before lumbar puncture as sepsis is deadly

115
Q

Epilepsy

A

Umbrella term for a condition where there is a tendency to have seizures

Transient episodes of abnormal electrical activity in the brain

116
Q

Anti-convulsants that induce hepatic enzymes

A

Carbamazepine, oxcarbazepine, phenobarbitol, phenytoin, primidone, topiramate

117
Q

Generalised Tonic-Clonic Seizures signs/symptoms

A
  • Loss of consciousness and tonic (tensing) and clonic (jerky)
  • tongue biting, urinary incontinence, groaning and irregular breathing
  • prolonged post-ictal period
118
Q

Generalised Tonic-Clonic Seizures Management

A

1st line: Sodium Valproate

2nd line: Lamotrigine or carbamazepine

119
Q

Absence seizures signs/symptoms

A

patient becomes blank, stares into space and abruptly becomes normal
- 10-20 seconds, unaware of their surrounds

120
Q

Absence seizures management

A

1st line: Sodium valproate or ethosuximide

2nd line: Lamotrigine

121
Q

Atonic seizures

A

drop attacks, indicate of lennoz-gastuat syndrome

- brief lapses in muscle tone

122
Q

Atonic seizures Mx

A

Sodium valporate

2nd line: lamotrigine

123
Q

Myoclonic seizures

A

sudden brief muscle contractions, like a sudden “jump”.

remains awake

124
Q

Myoclonic seizures Mx

A

1st line: Sodium Valproate

2nd line: Lamotrigine , levetiracretam, clonzaepam or topiramate

125
Q

Infantile spasms

A

Prednisolone or vigabatrin

126
Q

Focal seizures

A

Structural cause - affect speech, hearing, memory and emotions

127
Q

Focal seizures signs/symptoms

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

128
Q

Focal seizures Mx

A

1st Line: Carbamazepine or Lamotrigine
- Levetiracetam or oxcarbazepine if childbearing

2nd line: Sodium valproate or levetriracetam

129
Q

Status epilepticus

A

Recurrent epileptic seizures without full recovery of consciousness

It is a medical emergency. Uncontrolled glutamate release, excitotoxicity and neuronal death

It is defined as seizures lasting more than 5 minutes or more than 3 seizures in one hour (start treating after 10 minutes)

130
Q

Status epilepticus types

A

Generalized convulsive status epilepticus without cessation (most dangerous)

Non convulsive status: conscious but in “altered state”

Epilepsia partialis continua: continual focal seizures, consciousness preserved

131
Q

Status epilepticus Mx

A
  • ABCDE: High flow 02
  • check BG (50mls 50% glucose if hypo) and IV thiamine (if alcoholic)

Community or delay in IV: Diazepam (10-20mg) rectal or midazolam (5-10mg) buccal

IV access: lorazepam 4mg, repeated 10 minutes if seizure continues

If seizures persist: IV phenobarbital 15mg/kg IV or fosphenytoin or phenytoin

ITU: GA with thiopentone or propofol

132
Q

Functional attacks

A

not consciously mediated or no control of attacks

  • cordination is present, able to use direct language
  • outpatient EEG with video provocation
133
Q

Functional attacks Mx

A

Removal of any diagnosis of epilepsy
Withdrawal of antiepileptic drugs
Appropriate counselling for any previous traumatic events
Treatment of any associated anxiety or depression
CBT

134
Q

Neuropathic pain

A

Abnormal functioning of the sensory nerves delivering abnormal and painful signals to the brain.

135
Q

Causes of neuropathic pain

A
  1. Shingles
  2. Post herpatic neuralgia
  3. Trigeminal neuralgia
  4. MS
  5. Diabetic neuralgia
  6. CRPS
136
Q

Neuropathic pain Mx

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

137
Q

Trigeminal Neuralgia Mx

A

Carbamazepine

138
Q

Complex (chronic) Regional Pain Syndrome signs/symptoms

A

allodynia and hyperalgesia
swell, chnage colour, temp, flush with blood and abnormal sweating
hair and nail changes

139
Q

Facial Nerve branches

A
  1. Temporal
  2. Zygomatic
  3. Buccal
  4. Marginal Mandibular
  5. Cervical
140
Q

Facial nerve sensory, motor and parasympathetic

A
  • Motor: Supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.
  • Sensory: carries taste from the anterior 2/3 of the tongue.
  • Parasympathetic: it provides the parasympathetic supply to the submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).
141
Q

Bells Palsy

A

unilateral lower motor neurone facial nerve palsy

Reduced taste and hypersensitivity (stapedius palsy)

Patients unable to wrinkle their forehead (LMN) or whistle (buccinator)

Unilateral sagging of mouth, food stuck between gum and cheek, drooling of saliva and failure of eye closure

142
Q

Bells Palsy Mx

A
  • 50mg prednisolone for 10 days
  • or reducing regime
  • lubricating eye drops
143
Q

Ramsay-Hunt Syndrome

A

herpes zoster virus
unilateral LMN
painful tender vesicular rash in ear canal (extend anterior 2/3rd of tongue or hard palate)

144
Q

Ramsay-Hunt syndrome Mx

A

Prednisolone

Aciclovir

145
Q

Main symptoms of brain tumours when big

A
  1. Headaches - worse lying down, N&V due to raised ICP
  2. Progressive focal neurological deficits
  3. Seizures
  4. Gradual cognitive slowing and personality changes
  5. Endocrine disturbances
146
Q

Frontal tumour presentation

A
  • Contralateral weakness due to deficit in the primary motor cortex.
  • Personality changes including disinhibition and cognitive slowing.
  • Urinary incontinence due to disruption of the micturition inhibition centre.
  • Gaze abnormalities if there is involvement of the frontal eye fields.
  • Expressive dysphasia/aphasia for left sided lesions if Broca’s area is involved.
  • Seizures.
147
Q

Temporal

A
  • Memory
  • Receptive aphasia
  • contralateral superior quadrantopia
  • seizures
148
Q

Parietal lobe signs/symptoms

A

Contralateral weakness and sensory loss due to deficit in the primary somatosensory cortex

Contralateral inferior quadrantopia.

Dyscalculia 
dysgraphia 
Finger agnosia 
left-right disorientation 
Neglect
149
Q

ICP signs - raised

A 
altered mental state
visual field defects 
seizures 
unilateral ptosis 
3 and 4th nerve palsies 
Papilloedema
150
Q

Pilocytic astrocytoma

A

benign, slow growing, children

  • optic nerve, hypothalamic gliomas
  • cerebellum, brainstem
151
Q

Pilocytic astrocytoma Mx

A

Surgery

Radiotherapy - only in reoccurrence

152
Q

Low grade astrocytomas or diffuse

A

temporal lobe, posterior frontal and anterior Parietal

153
Q

Low grade astrocytomas or diffuse Mx

A

Surgery + chemo + radiotherapy

154
Q

Malignant astrocytomas (anaplastic vs glioblastoma multiforme)

A

arise in the cerebral hemispheres, most commonly temporal, parietal and frontal lobes

155
Q

Malignant astrocytomas (anaplastic vs glioblastoma multiforme) Ix & Mx

A

Glioblastoma: areas of necrosis and butterfly appearance

Surgery +radio + chemo (TMZ)

156
Q

Oligodendroglia tumours

A

frontal lobes - white matter and cortex

  • invade subarachnoid space (toothpaste )
  • calcification of CT scan - helps differ between astrocytomas
157
Q

Oligodendroglia tumours Mx

A

Surgery + Chemotherapy + Radiotherapy

158
Q

Meningiomas

A

benign extra‐axial intracranial tumours that grow slowly, are well demarcated and usually do not infiltrate the brain.
originate from arachnoidal cap cells within the arachnoid membrane.

159
Q

Acoustic neuroma

A

schwann cells surrounding the vestibular portion of CN VIII nerve that innervates the inner ear.

160
Q

Acoustic neuroma signs/symptoms

A 
Unilateral SN hearing loss 
vertigo 
tinnitus 
balance 
facial nerve palsy
161
Q

Acoustic neuroma Mx

A

Serial observation: periodic neuro exam, hearing aid and periodic MRI.

Stereotactic radiosurgery: involves image-guided accurate delivery of radiation to small volumes of brain, to reduce area subjected to radiation.

Microsurgical excision: surgery is performed via a retrosigmoid approach in the prone position

162
Q

Medulloblastoma

A

children and midline of cerebellum (below tentorium cerebellum)
- can disrupt CSF flow - hydrocephalus

163
Q

Pineal tumours

A 
Germinomas 
Non- germinomas 
 - teratoma 
- yolk sac
- choriocarcinoma 
- embryonal carcinoma
164
Q

Pineal tumours Mx

A

Shunt - VP or ETV

165
Q

Duchenne muscular dystrophy

A 
x linked recessive condition 
weakness 3-5 years in pelvic muscles 
Gowers signs 
calf hypertrophy 
toe walking 
exaggerated lumbar lordosis
166
Q

Spinal Muscular Dystrophy

A

rare autosomal recessive condition (SMN1 gene - chromosome 5) that causes a progressive loss of motor neurones, leading to progressive muscular weakness.

Spinal muscular atrophy affects the lower motor neurones in the spinal cord. This means there will be lower motor neurone signs, such as fasciculations, reduced tone

167
Q

TS

A

genetic condition that causes features in multiple systems. The characteristic feature is the development of hamartomas (benign neoplastic growths of the tissue that they origin from)

Affects the skin, brain, heart, lungs, kidneys and eyes

TSC1 (chromosome 9): hamartin
TSC2 (chromosome 16): tuberin

168
Q

TS signs/symptoms (skin)

A
  1. Ash leaf spots
  2. Shagreen patches
  3. Angiofibromas
  4. Subungual fibromata
  5. Cafe-au-lait spots
  6. Poliosis
169
Q

TS other signs

A

• Rhabdomyomas in the heart
• Gliomas (tumours of the brain and spinal cord)
• Polycystic kidneys
Lymphangioleimyomatosis (abnormal growth in smooth muscle cells, often affecting the lungs)
• Retinal hamartomas

170
Q

Myasthenia Gravis

A

Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.

Link with thymoma

171
Q

MG pathology

A

acetylcholine receptor antibodies - bind to postsynaptic NMJ receptor and block
- activate complement and damage post synaptic membrane cells

172
Q

MG signs/symptoms

A

min in morning and worse in evening

  • diplopia
  • dysphagia
  • ophthalmoplegia
  • ptosis
  • weakness in facial movements
  • fatigue in jaw when chewing
  • slurred speech
173
Q

MG diagnosis

A
  • repeated blinking - ptosis
  • prolonged upward gaze - diplopia
  • repeated abduction of one arm 20 times - unilateral weakness

ACh-R antibodies
MuSK antibodies
LRP4 antibodies

CT/MRI of thymus gland

edrophonium test (neostigimine) -

174
Q

MG management

A
  1. Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
  2. Immunosuppression e.g. prednisolone or azathioprine/mycophenolate
  3. Thymectomy
  4. Rituximab and Eculizumab
175
Q

MG crisis Mx

A
  1. non-invasive ventilation with BiPAP or full intubation and ventilation.
  2. Medical treatment of myasthenic crisis is with immunomodulatory therapies such as IV immunoglobulins and plasma exchange.
176
Q

Lambert Eaton Myasthenic Syndrome

A

It is a result of antibodies produced by the immune system against voltage-gated calcium channels on the presynaptic membrane

  • occurs in lung cancers or autoimmune
177
Q

Signs/symptoms of Lambert

A

proximal muscles are most notably affected, causing proximal muscle weakness and gait issues (gait before eyes)

diplopia, ptosis, slurred speech and swallowing problems

178
Q

Lambert - Mx

A

Amifampridine allows more acetylcholine to be released in the neuromuscular junction synapses. Treatment with 3- 4 diaminopyridine

  • immunosuppression (pred or azathioprine)
  • IV immunoglobulins
  • Plasmapheresis
179
Q

Charcot-Marie-Tooth Disease/Hereditary sensory motor neuropathy

A

affects the peripheral motor and sensory nerves (myelin or axons)

  • pes cavus
  • inverted champagne bottle legs
  • loss of ankle dorsiflexion (foot drop)
  • weakness of hands
  • reduced tendon reflexes
  • reduced muscle tone
  • peripheral sensory loss
180
Q

Guillian Barre Syndrome

A
  • acute paralytic polyneuropathy
  • acute, symmetrical, ascending weakness and can also cause sensory symptoms.
  • triggered by an infection (post viral) and is particularly associated with to campylobacter jejuni, cytomegalovirus and Epstein-Barr virus.
181
Q

Guillian Barre Syndrome Mx

A

IV immunoglobulins
Plasma exchange
VTE prophylaxis
severe: intubation, ventilation

182
Q

NF1 chromosome

183
Q

NF1 diagnosis

A

C – Café-au-lait spots (6 or more) measuring ≥ 5mm in children or ≥ 15mm in adults

R – Relative with NF1

A – Axillary or inguinal freckles (in groin or armpit)

BB – Bony dysplasia such as Bowing of a long bone or sphenoid wing dysplasia

I – Iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris

N – Neurofibromas (2 or more) or 1 plexiform neurofibroma

G – Glioma of the optic nerve

184
Q

NF2 chromosome

A

22 (codes for merlin - important for schwann cells)

185
Q

Lumbar herniation signs/symptoms

A

Radiculopathy: dysfunction of a nerve root causing a dermatomal sensory deficit with weakness of the muscle groups supplied by that nerve.

Sciatica: pain along the sciatic nerve usually due to compression of its nerve roots (L4-S3).

186
Q

L5/S1 prolapsed intervertebral disc

A
  1. Pain along the posterior thigh with radiation to the heel.
  2. Weakness of plantar flexion (on occasion).
  3. Sensory loss in the lateral foot.
  4. Reduced or absent ankle jerk.
187
Q

L4/5 prolapsed intervertebral disc

A

Pain along the posterior or posterolateral thigh with radiation to the dorsum of the foot and great toe.

Weakness of dorsiflexion of the toe or foot.

Paraesthesia and numbness of the dorsum of the foot and great toe.

Reflex changes unlikely.

188
Q

L3/4 prolapsed intervertebral disc

A
  1. Pain in the anterior thigh.
  2. Wasting of the quadriceps muscle.
  3. Weakness of the quadriceps function and dorsiflexion of foot.
  4. Diminished sensation over anterior thigh, knee and medial aspect of lower leg.
  5. Reduced knee jerk.
189
Q

Lumbar herniation Mx

A

Failure of conservative treatment (physiotherapy and analgesia)

Pain

Central disc prolapse: Patients with bilateral sciatica or other features indicating a central disc prolapse, such as sphincter disturbance and diminished perineal sensation, should be investigated promptly.

Tumour

Neurological deficits

190
Q

Cauda equina syndrome causes

A 
Prolapsed lumbar disc 
tumour compression 
trauma 
infection
haematoma
191
Q

Cauda equina symptoms/signs

A

urinary retention
saddle ananesthesia
urinary incontinence
low back pain and bilateral sciatic leg pain

192
Q

Lumbar spinal stenosis

A

narrowing of the spinal canal which compresses the lowest most spinal cord, conus medullaris, nerve roots, the latest will lead to symptoms of neurogenic claudication.

193
Q

Lumbar spinal stenosis causes

A

hypertrophy of facets joints and ligamentum flavum

protruding intervertebral discs

spondylolisthesis

osteophytes

194
Q

Lumbar stenosis signs/symptoms

A

insidious and progressive disease occurring over many months or years

Unilateral or bilateral hip, buttocks or lower extremity pain or burning sensation precipitated by standing or back extension and relieved by sitting, lumbar flexion or walking uphill (patients can often develop an “anthropoid posture” which is exaggerated flexion of the waist).

Neurogenic intermittent claudication: leg weakness, tingling and numbness which can be accompanied by paraesthesia.

195
Q

Cervical radiculopathy

A

compression or irritation of either or both of the dorsal (sensory) and ventral (motor) roots of a cervical nerve at one or more vertebral levels.

Compression can result from intervertebral disc herniation, osteophyte formation, or other mass effects near the exit foramen of the cervical spine. This results in lower motor neurone symptoms and often presents with arm pain, weakness, and/or sensory loss, with or without associated neck pain

196
Q

Cervical myelopathy

A

Cervical myelopathy is spinal cord dysfunction due to compression caused by narrowing of the spinal canal. Common causes include disc herniation, spondylosis, and congenital stenosis, often in combination.

The compression causes upper and lower motor and sensory neurone symptoms of the arms and legs, and the onset is often insidious.

197
Q

Cervical spondylosis clinical features

A

Radiculopathy

Myelopathy

198
Q

Degenerative Cervical myelopathy signs/symptoms

A

Imbalance and disturbance of gait which can lead to falls (due to hypertonia causing spasticity and decreased proprioception).

“Clumsy hands” with difficulty holding a fork or buttoning shirts, often with a tingling sensation in the fingertips.

Urinary or faecal incontinence (rare).

Pain in a non-dermatomal distribution

199
Q

Brown-Sequard Syndrome

A

Ipsilateral upper motor neuron paralysis and loss of proprioception below the lesion (ipsilateral motor and dorsal column sensory)

Contralateral loss of pain and temperature sensation beginning at 1 or 2 segments below the lesion (contralateral spinothalamic sensory level)

200
Q

Central cord syndrome causes

A
  • Acute extension injury to already stenotic neck
  • Syringomyelia
  • Tumour
201
Q

Central cord syndrome pathology and signs/symptoms

A

The fibers supplying the upper limbs in the lateral corticospinal tracts are more medial to the fibers supplying the lower limbs, hence a lesion in the central cord is more likely to damage the upper limb fibers

  • bilateral upper limb weakness>lower limb
  • “Cape-like” spinothalamic sensory loss
  • Dorsal Columns preserved
202
Q

Anterior cord syndrome

A

cord infarction - anterior spinal artery
-paralysis and loss of pain and temperature (anterior commissure for spinothalamic) below the level of injury with preserved proprioception and vibration sensation

203
Q

Hydrocephalus

A

Accumulation of excessive CSF within ventricular system of the brain

  1. Overproduction of CSF (v. rare tumours of choroid plexus)
  2. Obstruction to flow of CSF (inflammation, pus and tumours)
  3. Decreased resorption of CSF (post SAH or meningitis)
204
Q

Non-communicating vs communicating hydrocephalus

A

Non-communicating: obstruction to flow of CSF occurs within ventricular system

  • is that the fourth ventricle is small in comparison to the third and lateral ventricles.
  • Obstruction can be due to tumours compressing the ventricles, a colloid cyst obstructing the third ventricle can be seen or stenosis of the aqueduct.

Communicating: obstruction to flow of CSF outside of the ventricular system e.g. in subarachnoid space or at the arachnoid granulations (subarachnoid haemorrhage or meningitis)

205
Q

Hydrocephalus ex vacuo

A

Dilation of the ventricular system and compensatory increase in CSF volume secondary to loss of brain parenchyma e.g. AD disease

206
Q

Congenital hydrocephalus

A

Aqueductal stenosis

type 2 Arnold-Chiari malformations

spina bifida

207
Q

Hydrocephalus Mx

A

VP shunt or endoscopic third ventriculostomy

208
Q

Normal pressure hydrocephalus

A

Build-up of cerebrospinal fluid (CSF) due to an impaired resorption at the arachnoid granulations or overproduction of CSF.

  • idiopathic (Most common) but occurs secondary to meningitis, trauma or SAH
209
Q

Normal pressure hydrocephalus signs/symptoms

A

Apraxia of gait (shuffling gait)
Dementia
Urinary incontinence: detrusor overactivity

210
Q

Normal pressure hydrocephalus Mx

211
Q

Causes of raised ICP

A
  1. Obstruction: masses and chiari syndrome
  2. Increased production: choroid plexus papilloma
  3. Decreased absoption: SAH, meningitis
  4. Focal SOL
212
Q

Uncal herniation

A

medial temporal lobe herniating through tentorium

  • The first symptom is pupillary dilatation due to involvement of the ipsilateral oculomotor nerve.
  • The herniated uncus further compresses the pyramidal tracts in the crus cerebri, causing contralateral hemiparesis.
213
Q

Subfalcine herniation

A

herniation of the cingulate gyrus below the falx cerebri

- compression of the ipsilateral anterior cerebral artery, causing weakness in lower extremities.

214
Q

Tonsilar herniation

A

displacement of the cerebellar tonsils into the foramen magnum (posterior fossa lesion or arnold-chiari malformation)

215
Q

Central herniation

A

Brainstem: diplopia due to 6th CNVI and brainstem dysfunction

216
Q

Chiari Malformations

A

congenital or acquired malformations of the hindbrain affecting the structural relationships between the cerebellum, medulla and upper cervical spinal cord which causes impaired CSF circulation through the foramen magnum

217
Q

Chiari I malformation

A
  • most common
  • caudal displacement of the cerebellar tonsils below the foramen magnum
  • associated syringomyelia (an expanding cystic cavity or syrinx forming in the spinal cord that can cause damage to the central spinal cord).
218
Q

Chiari II malformation (Arnold-Chiari)

A

caudal displacement of the cerebellum and medulla below the foramen magnum with herniation of the fourth ventricle.
clear association with myelomeningocoele (spina bifida).

hydrocephalus and syringomyelia (common)

219
Q

Idiopathic intracranial hypertension

A

raised intracranial pressure with the absence of any space-occupying lesions or hydrocephalus

young childbearing females and obese patients

220
Q

Idiopathic intracranial hypertension signs/symptoms

A 
Headache 
papilloedema 
N&V
CN VI
double vision 
tinnitus 
radicular pain
221
Q

IIH Mx

A

Weight loss (obese), diuretics (acetazolamide and topiramtae)
VP shunt
Interventional radiology
- Intracranial venous sinus plasty
- Intracranial venous sinus stenting: you can’t take out

222
Q

Coup vs contra-coup injury

A

Coup: occurs to the brain on the side of the impact: compressive strain and tissue disruption

Contracoup – diametrically opposite point of impact

  • Denser CSF moves to impact (coup) zone first
  • Low pressure in brain moving away from zone creates cavitation bubbles damaging the parenchyma
223
Q

Diffuse axonal injury

A

Occurs at moment of injury

Affects central areas: Brainstem, Corpus collosum, parasagittal areas, Interventricular septum and hippocampal formation

Reduced consciousness and coma and if severe enough – vegetative state

224
Q

Parasomnias

A

Parasomnias are disruptive sleep-related disorders that can occur during arousals from REM sleep or partial arousals from NREM sleep

225
Q

Non-REM sleep

A

first 2/3rds of night

  • non dreaming
  • confusional arousal
  • sleep walking
  • bruxism
  • restless legs and PLMS
226
Q

REM sleep

A

latter third of night
• Often seen preceding Parkinson’s disease
• Idiopathic: don’t get the usual relaxation of the muscles
• Dreaming
• Much simpler behavior

227
Q

Narcolepsy (Gelinaeaus syndrome)

A

chronic sleep disorder characterized by overwhelming daytime drowsiness and sudden attacks of sleep. People with narcolepsy often find it difficult to stay awake for long periods of time, regardless of the circumstances. Narcolepsy can cause serious disruptions in your daily routine.

228
Q

Narcolepsy signs/symptoms

A 
Daytime sleepiness 
Cataplexy 
Hypnagogic hallucinations 
Sleep paralysis 
REM sleep disorder
229
Q

Narcolepsy Ix

A

`1. Overnight polysomnography

  1. Multiple sleep latency test
  2. Lumbar Puncture
230
Q

Narcolepsy Mx

A

Stimulants e.g. methylphenidate may cause dependence +/- psychosis

modafinil maybe be better. S/E: anxiety, aggression, dry mouth

231
Q

Adie’s pupil

A

loss of postganglionic parasympathetic innervation (constriction) to the iris sphincter and ciliary muscle (damage to ciliary ganglion).

  1. Anisocoria (large pupil) and blurring on near vision
  2. Light reflex absent
  3. Diminished or absent deep tendon reflex of lower limbs + Adie’s pupil +/- orthostatic hypotension = Holmes-Adie syndrome
232
Q

Adie’s pupil Ix

A

0.125% (low dose) of topical pilocarpine (cholinergic agonist) into both eyes. Adie’s pupil constricts (due to denervation hypersensitivity) while normal pupil doesn’t.

233
Q

Argyll Robertson

A

bilateral, irregular and small pupils. Both do not react to light however they constrict normally on accommodation

234
Q

3rd nerve palsy clinical features

A
  1. Ptosis
  2. Dilated pupil and accommodation abnormality
  3. Abduction and depression - primary position
235
Q

3rd palsy causes

A

Medical: hypertension, diabetes (pupil sparing)

Surgical: posterior communicating artery aneurysm, trauma and uncal herniation

236
Q

4th nerve palsy clinical features

A

Vertical diplopia: worse on looking down
Hypertropia: IO pulls it up
Depression: SO not working
Compensatory head tilt

237
Q

4th cranial nerve palsy causes

A

congenital or trauma

238
Q

6th clinical features

A

Horizontal double vision: worse on looking at distant targets.

Esotropia (eye turns inward) in primary position.

Abduction is limited

239
Q

6th causes

A

diabetes and hypertension (microvascular)

increased ICP (MAIN ONE)

240
Q

Cavernous sinus syndrome

A

lateral wall of the sinus contains cranial nerves 3,4 and 5 (V1 and V2).

While the internal carotid artery (with the sympathetic system) and cranial nerve 6 passes through the cavernous sinus.

241
Q

Cavernous sinus syndrome signs/symptoms

A

Ptosis and ophthalmoplegia: due to compression of cranial nerves 3,4 and 6

Loss of corneal reflex: due to cranial nerve 5 (V1) involvement

Maxillary sensory loss: due to cranial nerve 5 (V2) involvement

Horner’s syndrome: due to involvement of internal carotid ocular sympathetic

Proptosis and periorbital swelling: due to increased venous pressure in the veins draining the orbit

242
Q

Tension headaches

A

muscle ache in the frontalis, temporalis and occipitalis muscles.

  • Tension headaches comes on and resolve gradually and don’t produce visual changes.
  • midl ache across forehead and in band like pattern
  • absence of N&V, photophobia and phonophobia
243
Q

Tension headaches Mx

A

• Basic analgesia e.g. paracetamol
• Relaxation physiotherapy of scalp muscles
o Reduce stress levels, avoid alcohol
o Hot towels to local area
• Antidepressant: Dothiepin or amitriptyline: 3 months RX

244
Q

Trigeminal Neuralgia cause and triggers?

A

compression of the nerve (V2/V3)

cold weather, spicy food, caffeine and citrous fruits

245
Q

TN signs/symptoms

A

intense stabbing unilateral facial pain that comes on spontaneously and last anywhere between a few seconds to hours.

Frequency: 10-100

246
Q

TN Mx

A

Carbamazepine
- gabapentin, phenytoin and baclofen
Surgery

247
Q

Migraine Dx

A

2 of moderate/severe unilateral, throbbing pain, worst on movement

1 of autonomic features, photophobia or phonophobia, N&V

248
Q

Migraine pathophysiology

A

Both vascular and neural influences (migraine centre in dorsal raphe nucleus) causes migraines in susceptible individuals (activation of trigeminal vascular system)

Blood vessels constrict and dilate: sensed by dura CN V

249
Q

Migraine signs/symptoms

A
  1. The prodromal stage
  2. Premonitory or prodromal stage
  3. Aura (lasting up to 60 minutes) e.g. sparks in vision, blurring, lines across
  4. Headache stage (lasts 4-72 hours)
    - Moderate to severe intensity
    - Pounding or throbbing in nature
    - Usually unilateral but can be bilateral
    - Photophobia
    - Phonophobia
    - Nausea and vomiting
    - Pre-syncope/syncope
  5. Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping)
  6. Postdromal or recovery phase
250
Q

Acute management of migraine

A

Dark and quiet room

  1. Aspirin (900mg)
  2. Paracetamol (1g)
  3. NSAIDs e.g. ibuprofen or naproxen
  4. Triptans e.g. Rizatriptan and sumatriptan (50mg)
  5. gastroparesis or vomiting consider antiemetic e.g. metoclopramide
251
Q

Prophylaxis of migraine

A
  1. Avoiding triggers and headache diary can reduce the frequency of the migraine.
  2. Amitriptyline: 10-25mg (max 75mg) give at night
  3. Propranolol: non-selective: 80mg
  4. Topiramate (this is teratogenic and can cause a cleft lip/palate so patients should not get pregnant): be careful in childbearing age
  5. Candesartan (16mg): unlicensed
252
Q

Trigeminal autonomic cephalgias

A

primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids
- 4 types are cluster, paroxysmal hemicrania, hemicrania continua, SUNCT

253
Q

Ipsilateral cranial autonomic features

A 
Ptosis 
Miosis 
Nasal stuffiness 
Nausea/vomiting 
Tearing 
Eye lid oedema
254
Q

Cluster headaches

A
  • severe and unbearable unilateral headaches, usually around the eye.
  • suffer 3 – 4 attacks a day for weeks or months followed by a pain free period lasting 1-2 years.
  • alcohol, strong smells and exercise
255
Q

Cluster headaches signs/symptoms

A 
45-90 mins of 1-8 times per day 
Red, swollen and watering eye
miosis
ptosis
Nasal discharge
Facial sweating
256
Q

Cluster headaches Ix and Mx (acute)

A

MRI brain and MR angiogram

  • Triptans e.g. sumatriptan 6mg injected subcutaneously
  • High flow O2
257
Q

Cluster headaches Prophylaxis

A

Verapamil
Lithium
Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)

258
Q

Paroxysmal hemicrnaia or Hemicrania continua

A

Shorter duration and more frequent than cluster

  • duration 10-30 mins
  • frequency 1-40 per day
259
Q

Paroxysmal hemicrnaia or Hemicrania continua Mx

A

absolute response to indormethicin (NSAID)

260
Q

SUNCT

A 
S = Short lived (15-120 seconds)
U = Unilateral 
N = Neuralgiaform headache 
C = conjunctival injections 
T = tearing
261
Q

SUNCT Mx

A
  1. Lamotrigine

2. Gabapentin

Medical Diseases (18 decks)

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