Neurology disease summaries Flashcards
(261 cards)
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
2
Q
CVA types
A
Infraction/Ischaemia
- thrombus formation or embolus (cardioembolic/thromboembolic)
- atherosclerosis
- shock
- vasculitis
Intracranial haemorrhage
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
4
Q
stroke symptoms
A
- Sudden weakness of limbs: initially flaccid and then spastic (UMN)
- Sudden facial weakness
- Sudden onset dysphasia (speech disturbance)
- Sudden onset visual or sensory loss e.g. homonymous hemianopia
5
Q
TACS
A
- Unilateral weakness (and sensory deficit) of face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction e.g. dysphasia, visuospatial disorders)
Emboli
6
Q
PACS
A
Two of the following:
- Unilateral weakness (and sensory deficit) of face, arm and leg
- Homonymous hemianopia
- Higher cerebral dysfunction e.g. dysphasia, visuospatial disorders)
7
Q
LACS
A
One:
Pure sensory
Pure motor
sensori-motor
ataxic hemiparesis
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
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
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
11
Q
TIA
A
Defined as transient neurological dysfunction secondary to ischaemia (lack of blood flow) without infarction (death of tissues).
12
Q
TIA management
A
- Aspirin 300mg daily
- clopidogrel
- Carotid endarterectomy
13
Q
Receptive dysphagia
A
is difficulty in comprehension: Wernickes area (superior temporal)
14
Q
Expressive dysphagia
A
difficulty in putting words together to make meaning: Broca Area (frontal)
15
Q
intracranial bleeds signs/symptoms
A
Seizures
Focal weakness
Vomiting
Reduced consciousness`
Other sudden onset neurological symptoms
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
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.
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.
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
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
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).
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.
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
24
Q
SDH management
A
prevent secondary insults
- hypoxia, hypotension and mass lesions
- control ICP and CPP
Craniotomy or burr hole washout
25
Raised ICP medical management and surgical
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
26
EDH
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
27
EDH signs/symptoms
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
28
EDH diagnosis
CT scan they have a bi-convex shape and are limited by the cranial sutures
29
Intracerebral haemorrhage Iv
CT scan: Well demarcated intra-parenchymal haematomas
30
Intracerebral haemorrhage management
• 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
31
Subarachnoid Haemorrhage
bleeding into the subarachnoid space, where the cerebrospinal fluid is located. Between pia and arachnoid membrane
Usually an aneurysm
32
Subarachnoid Haemorrhage signs/symptoms
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)
33
Subarachnoid Haemorrhage Iv
CT
LP
Angiography (CT or MRI)
34
Subarachnoid Haemorrhage management
surgical: coiling or clipping
35
Subarachnoid Haemorrhage complications
vasospasm: prolonged arterial contraction - delayed ischaemic neurological deficit (3-14 days)
- nimodipine
rebleeding
SIADH: hyponatraemia
Hydrocephalus
antiepileptic medications
36
Arteriovenous malformations
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
37
Arteriovenous malformations Iv and management
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
38
Cavernous malformation
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
39
Cavernous malformation Ix
CT
| MRI: popcorn
40
Dural venous sinus thrombosis - most common
sagittal sinus thrombosis or transverse sinus thrombosis
41
Cortical sinus thrombosis
Usually occurs with a sinus thrombus as it extends into the cortical veins causing infarction in venous territory.
42
Multiple sclerosis
Chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system.
young adults and women
43
MS causes
Multiple genes, Epstein–Barr virus (EBV), Low vitamin D, Smoking, obesity, living near the equator
44
Pyramidal dysfunction
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
45
MS signs/symptoms
```
Pyramidal dysfunction
Optic neuritis
Sensory symptoms
LUTD
Cerebellar
Fatigue
Cognitive impairment
```
46
Optic neuritis
demyelination of the optic nerve and unilateral loss of vision
- central scotoma
- pain on eye movement
- impaired colour vision (dyschromatopsia)
- RAPD
47
MS: Disease patterns
Clinically isolated syndrome
relapsing/remitting
Secondary progressive
Primary progressive
48
MS Iv
over 1 year
2 episodes suggestive of demyelination and dissemination in time and place
LP: oligoclonal bands in CSF
49
Acute exacerbation/relapse MS treatment
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)
50
Optic neuritis acute management
IV methylprednisolone followed by oral prednisolone
51
Pyramidal dysfunction management (MS)
- Exercises
- Oral baclofen and Tizanidine
- Benzodiazepine
- B toxin in joints
- intrathecal baclofen/phenol
52
Sensory symptoms (MS) treatment
Anti-convulsant e.g. gabapentin
Anti-depressant e.g. amitriptyline
Tens machine
Acupuncture
Lignocaine infusion
53
LUTD management (MS)
Bladder drill (training)
Anti-cholinergic e.g. oxybutynin and tolterodine (worsen cognitive impairment)
Desmopressin e.g. long journey
Catheterisation e.g. significant retention
54
Disease modifying MS
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
55
Motor Neurone disease
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.
56
MND types
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
57
MND signs/symptoms
late middle aged (e.g. 60) man, possibly with an affected relative spastic gait, foot drop +/- proximal myopathy, weak grip and shoulder abduction
58
LMN signs/symptoms
o Muscle wasting
o Reduced tone
o Fasciculations (twitches in the muscles)
o Reduced reflexes
59
UMN signs/symptoms
```
o Increased tone or spasticity
o Brisk reflexes/hyperreflexia
o Upgoing plantar responses
o Spastic gait
o Exaggerated jaw jerk
o Slowed movements
```
60
Bulbar variant (Motor Neurone) management
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
61
Riluzole
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
62
Parkinson’s Disease
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
63
Parkinson’s Disease risk factors
```
Age – most important
Male sex – slight increase
Rural living – slight increase
Smoking – decreases risk
FH of Parkinson’s disease
Drugs - cyclizine or metaproclomide
```
64
Parkinson’s Disease signs/symptoms
PD: usually asymmetrical
1. Resting tremor (improves with movement)
2. Rigidity: Cogwheel
3. Bradykinesia (slower movements)
4. Postural disturbances
65
Other signs/symptoms of PD
```
Depression
Sleep disturbance and insomnia (lack of REM sleep?)
Loss of the sense of smell (anosmia)
Cognitive impairment and memory problems
GI dysfunction
```
66
PD should not present with
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
67
PD management
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
68
PD side effects of medication
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
69
Drug induced psychosis PD Mx
clozapine (agranulocytosis) and quetiapine
70
Vascular Parkinsonism
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
71
Vascular Park Iv
Poor levodopa response
Structural brain imaging will guide diagnosis
72
Drug Induced Parkinsonism Mechanism
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.
73
Drug Induced parkinsonism signs/symptoms
1. Symmetrical
2. Postural Tremor e.g. oustretched arms
3. Orolingual dyskinesias, tardive dystonia and akathisia
74
Drug induced parkinsonism mx
remove drug that blocks dopamine
75
benign essential tremor
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)
76
Benign essential tremor mx
to improve symptoms
1. propranolol
2. Primidone
77
Multi system atrophy
neurones of multiple systems of nerves in the brain to degenerate including basal ganglia
6th and 7th decade
78
Multi-system atrophy signs/symptoms
autonomic dysfunction (postural hypotension, constipation, abnormal sweating and sexual dysfunction) and cerebellar dysfunction (ataxia)
core triad: dysautonomia, cerebellar features and parkinsonism
79
Progressive supranuclear palsy
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.
80
Primary dementias
AZ, Picks, Lewy body, Huntington's
81
Alzheimer disease
Neurodegenerative proteinopathy (amyloid)
usually sporadic
Familial: APP (amyloid precursor), presenilin 1 & 2 and e4
82
Pathology of AD
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
83
AD Ix
clinical
MRI: temporal and parietal loss
SPECT: temporoparietal and reduced metabolism
CSF: Reduces amyloid and increase in tau
84
AD Mx
Cholinesterase inhibitors - rivastigmine, galantamine and donepezil
NMDA receptor blocker e.g. Menantine - protects against too much glutamate
85
Dementia with lewy bodies
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)
86
signs/symptoms of lewy body
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
87
Lewy Body Ix and Mx
Dat and alpha synuclein ligand imaging/a-synuclein in CSF
Mx
- small levodopa dose
- trial cholinesterase inhibitors
88
Parkinsons disease dementia
PDD >1 year of presentation
89
Huntington's chorea
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
90
Huntington's chorea pathology
loss of basal ganglia cells (basal ganglia, cuada and putamen) and cortex (frontal, parietal)
91
HC signs/symptoms
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
92
HD Mx
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.
93
Picks
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
94
Picks signs/symptoms
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
95
Picks Ix and Mx
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
96
Vascular dementia
sudden onset and stepwise deterioration
97
Multi infarct dementia
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
98
Multi-infarct dementia Ix
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
99
Functional Cognitive impairment
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)
100
Prion disease
Most common human prion disease = Creutzfeldt-jakob disease
Natually occuring PrPc (everyone has it) – misfolded PrPsc = neurodegeneration
Most concentrated in CNS and lymphatics
101
Prion disease types
- sporadic
- variant: Bovine spongiform encephalopathy
- iatrogenic
- genetic
102
Transient global amnesia
- 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
103
Transient epileptic amnesia
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.
104
Transient epileptic amnesia
complex activities with no recollection events
105
Meningitis causes with ages (bacteria)
- 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
Viral meningitis types
HSV, VZV and enterovirus
107
Meningitis signs/symptoms
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
Meningitis Ix
```
Kernig's test
Brudzinskis test
Blood cultures
Throat swab
Blood EDTA PCR
CSF LP
```
109
Meningitis Mx
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
Prophylaxis Meningitis Mx
Ciprofloxacin 500mg
111
aspectic meningitis
non-pyogenic bacterial meningitis
o A low number of WBC
o A minimally elevated protein
o A normal glucose
112
Encephalitis
inflammation of brain
| - commonly viral, HSV1/2, VZV (chickenpox), cytomegalovirus (immunodeficiency), EBV
113
Encephalitis signs/symptoms
```
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
Encephalitis Mx
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
Epilepsy
Umbrella term for a condition where there is a tendency to have seizures
Transient episodes of abnormal electrical activity in the brain
116
Anti-convulsants that induce hepatic enzymes
Carbamazepine, oxcarbazepine, phenobarbitol, phenytoin, primidone, topiramate
117
Generalised Tonic-Clonic Seizures signs/symptoms
- Loss of consciousness and tonic (tensing) and clonic (jerky)
- tongue biting, urinary incontinence, groaning and irregular breathing
- prolonged post-ictal period
118
Generalised Tonic-Clonic Seizures Management
1st line: Sodium Valproate
| 2nd line: Lamotrigine or carbamazepine
119
Absence seizures signs/symptoms
patient becomes blank, stares into space and abruptly becomes normal
- 10-20 seconds, unaware of their surrounds
120
Absence seizures management
1st line: Sodium valproate or ethosuximide
2nd line: Lamotrigine
121
Atonic seizures
drop attacks, indicate of lennoz-gastuat syndrome
| - brief lapses in muscle tone
122
Atonic seizures Mx
Sodium valporate
| 2nd line: lamotrigine
123
Myoclonic seizures
sudden brief muscle contractions, like a sudden “jump”.
| remains awake
124
Myoclonic seizures Mx
1st line: Sodium Valproate
| 2nd line: Lamotrigine , levetiracretam, clonzaepam or topiramate
125
Infantile spasms
Prednisolone or vigabatrin
126
Focal seizures
Structural cause - affect speech, hearing, memory and emotions
127
Focal seizures signs/symptoms
Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot
128
Focal seizures Mx
1st Line: Carbamazepine or Lamotrigine
- Levetiracetam or oxcarbazepine if childbearing
2nd line: Sodium valproate or levetriracetam
129
Status epilepticus
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
Status epilepticus types
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
Status epilepticus Mx
- 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
Functional attacks
not consciously mediated or no control of attacks
- cordination is present, able to use direct language
- outpatient EEG with video provocation
133
Functional attacks Mx
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
Neuropathic pain
Abnormal functioning of the sensory nerves delivering abnormal and painful signals to the brain.
135
Causes of neuropathic pain
1. Shingles
2. Post herpatic neuralgia
3. Trigeminal neuralgia
4. MS
5. Diabetic neuralgia
6. CRPS
136
Neuropathic pain Mx
Amitriptyline
Duloxetine
Gabapentin
Pregabalin
137
Trigeminal Neuralgia Mx
Carbamazepine
138
Complex (chronic) Regional Pain Syndrome signs/symptoms
allodynia and hyperalgesia
swell, chnage colour, temp, flush with blood and abnormal sweating
hair and nail changes
139
Facial Nerve branches
1. Temporal
2. Zygomatic
3. Buccal
4. Marginal Mandibular
5. Cervical
140
Facial nerve sensory, motor and parasympathetic
* 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
Bells Palsy
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
Bells Palsy Mx
- 50mg prednisolone for 10 days
- or reducing regime
- lubricating eye drops
143
Ramsay-Hunt Syndrome
herpes zoster virus
unilateral LMN
painful tender vesicular rash in ear canal (extend anterior 2/3rd of tongue or hard palate)
144
Ramsay-Hunt syndrome Mx
Prednisolone
| Aciclovir
145
Main symptoms of brain tumours when big
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
Frontal tumour presentation
- 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
Temporal
- Memory
- Receptive aphasia
- contralateral superior quadrantopia
- seizures
148
Parietal lobe signs/symptoms
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
ICP signs - raised
```
altered mental state
visual field defects
seizures
unilateral ptosis
3 and 4th nerve palsies
Papilloedema
```
150
Pilocytic astrocytoma
benign, slow growing, children
- optic nerve, hypothalamic gliomas
- cerebellum, brainstem
151
Pilocytic astrocytoma Mx
Surgery
| Radiotherapy - only in reoccurrence
152
Low grade astrocytomas or diffuse
temporal lobe, posterior frontal and anterior Parietal
153
Low grade astrocytomas or diffuse Mx
Surgery + chemo + radiotherapy
154
Malignant astrocytomas (anaplastic vs glioblastoma multiforme)
arise in the cerebral hemispheres, most commonly temporal, parietal and frontal lobes
155
Malignant astrocytomas (anaplastic vs glioblastoma multiforme) Ix & Mx
Glioblastoma: areas of necrosis and butterfly appearance
| Surgery +radio + chemo (TMZ)
156
Oligodendroglia tumours
frontal lobes - white matter and cortex
- invade subarachnoid space (toothpaste )
- calcification of CT scan - helps differ between astrocytomas
157
Oligodendroglia tumours Mx
Surgery + Chemotherapy + Radiotherapy
158
Meningiomas
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
Acoustic neuroma
schwann cells surrounding the vestibular portion of CN VIII nerve that innervates the inner ear.
160
Acoustic neuroma signs/symptoms
```
Unilateral SN hearing loss
vertigo
tinnitus
balance
facial nerve palsy
```
161
Acoustic neuroma Mx
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
Medulloblastoma
children and midline of cerebellum (below tentorium cerebellum)
- can disrupt CSF flow - hydrocephalus
163
Pineal tumours
```
Germinomas
Non- germinomas
- teratoma
- yolk sac
- choriocarcinoma
- embryonal carcinoma
```
164
Pineal tumours Mx
Shunt - VP or ETV
165
Duchenne muscular dystrophy
```
x linked recessive condition
weakness 3-5 years in pelvic muscles
Gowers signs
calf hypertrophy
toe walking
exaggerated lumbar lordosis
```
166
Spinal Muscular Dystrophy
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
TS
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
TS signs/symptoms (skin)
1. Ash leaf spots
2. Shagreen patches
3. Angiofibromas
4. Subungual fibromata
5. Cafe-au-lait spots
6. Poliosis
169
TS other signs
• 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
Myasthenia Gravis
Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.
Link with thymoma
171
MG pathology
acetylcholine receptor antibodies - bind to postsynaptic NMJ receptor and block
- activate complement and damage post synaptic membrane cells
172
MG signs/symptoms
min in morning and worse in evening
- diplopia
- dysphagia
- ophthalmoplegia
- ptosis
- weakness in facial movements
- fatigue in jaw when chewing
- slurred speech
173
MG diagnosis
- 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
MG management
1. Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
2. Immunosuppression e.g. prednisolone or azathioprine/mycophenolate
3. Thymectomy
4. Rituximab and Eculizumab
175
MG crisis Mx
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
Lambert Eaton Myasthenic Syndrome
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
Signs/symptoms of Lambert
proximal muscles are most notably affected, causing proximal muscle weakness and gait issues (gait before eyes)
diplopia, ptosis, slurred speech and swallowing problems
178
Lambert - Mx
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
Charcot-Marie-Tooth Disease/Hereditary sensory motor neuropathy
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
Guillian Barre Syndrome
- 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
Guillian Barre Syndrome Mx
IV immunoglobulins
Plasma exchange
VTE prophylaxis
severe: intubation, ventilation
182
NF1 chromosome
17 (AD)
183
NF1 diagnosis
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
NF2 chromosome
22 (codes for merlin - important for schwann cells)
185
Lumbar herniation signs/symptoms
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
L5/S1 prolapsed intervertebral disc
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
L4/5 prolapsed intervertebral disc
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
L3/4 prolapsed intervertebral disc
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
Lumbar herniation Mx
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
Cauda equina syndrome causes
```
Prolapsed lumbar disc
tumour compression
trauma
infection
haematoma
```
191
Cauda equina symptoms/signs
urinary retention
saddle ananesthesia
urinary incontinence
low back pain and bilateral sciatic leg pain
192
Lumbar spinal stenosis
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
Lumbar spinal stenosis causes
hypertrophy of facets joints and ligamentum flavum
protruding intervertebral discs
spondylolisthesis
osteophytes
194
Lumbar stenosis signs/symptoms
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
Cervical radiculopathy
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
Cervical myelopathy
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
Cervical spondylosis clinical features
Radiculopathy
| Myelopathy
198
Degenerative Cervical myelopathy signs/symptoms
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
Brown-Sequard Syndrome
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
Central cord syndrome causes
- Acute extension injury to already stenotic neck
- Syringomyelia
- Tumour
201
Central cord syndrome pathology and signs/symptoms
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
Anterior cord syndrome
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
Hydrocephalus
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
Non-communicating vs communicating hydrocephalus
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
Hydrocephalus ex vacuo
Dilation of the ventricular system and compensatory increase in CSF volume secondary to loss of brain parenchyma e.g. AD disease
206
Congenital hydrocephalus
Aqueductal stenosis
type 2 Arnold-Chiari malformations
spina bifida
207
Hydrocephalus Mx
VP shunt or endoscopic third ventriculostomy
208
Normal pressure hydrocephalus
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
Normal pressure hydrocephalus signs/symptoms
Apraxia of gait (shuffling gait)
Dementia
Urinary incontinence: detrusor overactivity
210
Normal pressure hydrocephalus Mx
VP shunt
211
Causes of raised ICP
1. Obstruction: masses and chiari syndrome
2. Increased production: choroid plexus papilloma
3. Decreased absoption: SAH, meningitis
4. Focal SOL
212
Uncal herniation
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
Subfalcine herniation
herniation of the cingulate gyrus below the falx cerebri
| - compression of the ipsilateral anterior cerebral artery, causing weakness in lower extremities.
214
Tonsilar herniation
displacement of the cerebellar tonsils into the foramen magnum (posterior fossa lesion or arnold-chiari malformation)
215
Central herniation
Brainstem: diplopia due to 6th CNVI and brainstem dysfunction
216
Chiari Malformations
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
Chiari I malformation
- 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
Chiari II malformation (Arnold-Chiari)
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
Idiopathic intracranial hypertension
raised intracranial pressure with the absence of any space-occupying lesions or hydrocephalus
young childbearing females and obese patients
220
Idiopathic intracranial hypertension signs/symptoms
```
Headache
papilloedema
N&V
CN VI
double vision
tinnitus
radicular pain
```
221
IIH Mx
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
Coup vs contra-coup injury
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
Diffuse axonal injury
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
Parasomnias
Parasomnias are disruptive sleep-related disorders that can occur during arousals from REM sleep or partial arousals from NREM sleep
225
Non-REM sleep
first 2/3rds of night
- non dreaming
- confusional arousal
- sleep walking
- bruxism
- restless legs and PLMS
226
REM sleep
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
Narcolepsy (Gelinaeaus syndrome)
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
Narcolepsy signs/symptoms
```
Daytime sleepiness
Cataplexy
Hypnagogic hallucinations
Sleep paralysis
REM sleep disorder
```
229
Narcolepsy Ix
`1. Overnight polysomnography
2. Multiple sleep latency test
3. Lumbar Puncture
230
Narcolepsy Mx
Stimulants e.g. methylphenidate may cause dependence +/- psychosis
modafinil maybe be better. S/E: anxiety, aggression, dry mouth
231
Adie's pupil
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
Adie's pupil Ix
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
Argyll Robertson
bilateral, irregular and small pupils. Both do not react to light however they constrict normally on accommodation
234
3rd nerve palsy clinical features
1. Ptosis
2. Dilated pupil and accommodation abnormality
3. Abduction and depression - primary position
235
3rd palsy causes
Medical: hypertension, diabetes (pupil sparing)
Surgical: posterior communicating artery aneurysm, trauma and uncal herniation
236
4th nerve palsy clinical features
Vertical diplopia: worse on looking down
Hypertropia: IO pulls it up
Depression: SO not working
Compensatory head tilt
237
4th cranial nerve palsy causes
congenital or trauma
238
6th clinical features
Horizontal double vision: worse on looking at distant targets.
Esotropia (eye turns inward) in primary position.
Abduction is limited
239
6th causes
diabetes and hypertension (microvascular)
increased ICP (MAIN ONE)
240
Cavernous sinus syndrome
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
Cavernous sinus syndrome signs/symptoms
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
Tension headaches
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
Tension headaches Mx
• 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
Trigeminal Neuralgia cause and triggers?
compression of the nerve (V2/V3)
cold weather, spicy food, caffeine and citrous fruits
245
TN signs/symptoms
intense stabbing unilateral facial pain that comes on spontaneously and last anywhere between a few seconds to hours.
Frequency: 10-100
246
TN Mx
Carbamazepine
- gabapentin, phenytoin and baclofen
Surgery
247
Migraine Dx
2 of moderate/severe unilateral, throbbing pain, worst on movement
1 of autonomic features, photophobia or phonophobia, N&V
248
Migraine pathophysiology
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
Migraine signs/symptoms
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
Acute management of migraine
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
Prophylaxis of migraine
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
Trigeminal autonomic cephalgias
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
Ipsilateral cranial autonomic features
```
Ptosis
Miosis
Nasal stuffiness
Nausea/vomiting
Tearing
Eye lid oedema
```
254
Cluster headaches
- 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
Cluster headaches signs/symptoms
```
45-90 mins of 1-8 times per day
Red, swollen and watering eye
miosis
ptosis
Nasal discharge
Facial sweating
```
256
Cluster headaches Ix and Mx (acute)
MRI brain and MR angiogram
- Triptans e.g. sumatriptan 6mg injected subcutaneously
- High flow O2
257
Cluster headaches Prophylaxis
Verapamil
Lithium
Prednisolone (a short course for 2-3 weeks to break the cycle during clusters)
258
Paroxysmal hemicrnaia or Hemicrania continua
Shorter duration and more frequent than cluster
- duration 10-30 mins
- frequency 1-40 per day
259
Paroxysmal hemicrnaia or Hemicrania continua Mx
absolute response to indormethicin (NSAID)
260
SUNCT
```
S = Short lived (15-120 seconds)
U = Unilateral
N = Neuralgiaform headache
C = conjunctival injections
T = tearing
```
261
SUNCT Mx
1. Lamotrigine
| 2. Gabapentin
