Neurology Conditions Flashcards

(180 cards)

1
Q

What is the normal intracranial pressure in adults?

A

<15mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does raised ICP cause damage?

A

Compression of the brain leads to reduced blood supply to the cells –> Ischaemia –> No ATP –> Failure of NaKATPase –> Raised Na –> water follow –> cytotoxic cellular oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What investigations would you request if you suspect raised ICP?

A

CT head
Lumbar Puncture - IF SAFE (no evidence of coning) to get an opening pressure
Glucose, renal function, electrolytes, clotting
Toxicology screen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does raised ICP present?

A
Headache
Vomiting
Change in consciousness
Seizures
Cushings reflex
Changes to pupils
Hemiparesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the trio of signs seen in Cushing’s reflex?

A

Hypertension - sympathetic stimulation
Bradycardia - baroreceptors detect raised BP
Bradypnoea/ Cheyne-stokes breathing - Ischaemia to resp centre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What changes are seen to the eyes in raised ICP?

A

Pupils constrict initially then dilate
Peripheral visual field loss
Papilloedema and loss of venous pulsation at the disk
CN 3 and 6 palsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the types of brain herniation?

A

Subfalcine/cingulate
Uncal
Tonsillar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens in a subfalcine/cingulate herniation and what does it cause?

A

Cingulate gyrus push under falx cerebri and compress anterior cerebral artery

  • Contralateral weakness - especially leg
  • Gait problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in an uncal herniation and what does it cause?

A

Uncus herniate through tentorial notch to compress:
CN3 = ipsilateral dilated, down and out
CN6 = diplopia when looking to side of lesion
Reticular formation - reduced GCS
Chemoreceptor trigger zone - N&V
Crus cerebri via kernohan’s notch - Ipsilateral hemiparesis
Ipsilateral PCA - contralateral homonymous hemianopia with macular sparing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens in a tonsillar herniation? What symptoms do you get?

A

Cerebellar tonsils herniate through foramen magnum leading to compression of brainstem.
Cardiorespiratory centres compressed - apnoea
Ataxia
CN6 palsy
Headache and neck stiffness
Flaccid paralysis
LOC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are brain herniations managed?

A
Raise end of bed to 30 degrees
IV Mannitol
IV Dexamethasone
Fluid restrict
Normothermia
Normoglycaemia 
Analgesia, sedation and anticonvulsants
Decompressive craniectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the most common types of venous sinus thrombosis?

A

Sagittal sinus

Transverse sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does sagittal sinus thrombosis present?

A
Headache - often sudden onset
Vomiting
Seizures
Hemiplegia
Decreased visual acuity
Papilloedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does transverse sinus thrombosis present?

A
Headache - often sudden onset
Mastoid pain
Focal CNS signs
Seizures
Papilloedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does sigmoid sinus thrombosis present?

A

Cerebellar signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does inferior petrosal sinus thrombosis present?

A

CN5&6 palsy

Retro-orbital pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What commonly causes cavernous sinus thrombosis?

A

Infection - facial pustules, folliculitis, sinusitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does cavernous sinus thrombosis present?

A
Headache
Peri-orbital pain and oedema
Proptosis
Ophthalmoplegia - CN6 first, then 3 and 4
Central retinal vein thrombosis
Hyperaesthesia of upper face (CN5)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes venous sinus thrombosis?

A

Hypercoaguable state - pregnancy, COCP, dehydration
Head injury
Tumours
Recent lumbar puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the differentials for venous sinus thrombosis?

A

Subarachnoid haemorrhage
Arterial infarct
Meningitis
Abscess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is venous sinus thrombosis managed?

A

Anticoagulate - IV heparin or LMWH then warfarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the complications associated with venous sinus thrombosis?

A

Transtentorial herniation due to mass effect or oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How would a venous sinus thrombosis appear on CT with contrast?

A

Empty delta sign - superior sagittal sinus should usually fill with contrast but doesn’t when thrombosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What characteristics of a headache indicate it may be due to a space occupying lesion?

A

Worse on:

  • Waking
  • Lying down
  • Bending forward
  • Coughing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What symptom would mean space occupying lesions must be excluded as a cause?
Adult onset seizures - especially if aura (focal or localising) or post ictal weakness
26
What can cause a space occupying lesion?
Metastatic tumours - breast, lung, melanoma Primary tumour - astrocytoma, glioblastoma, oligodendroglioma, meningioma Aneurysm Abscess Chronic subdural haematoma Granuloma Cyst
27
What are the risk factors for idiopathic intracranial hypertension?
Obese Female 30's COCP Others - steroids, tetracyclines, vit A, lithium
28
How does idiopathic intracranial hypertension present?
``` Headache Narrowed visual fields Blurred vision and diplopia CN6 palsy Enlarged blind spot - papilloedema No change in cognition and consciousness ```
29
How is idiopathic intracranial hypertension managed?
``` Weight loss Acetazolamide or topiramate Prednisolone Optic nerve sheath fenestration (reduce pressure on optic nerve head) LP shunt ```
30
What is a hydrocephalus?
Excess volume of CSF fluid within ventricles due to imbalance of production and absorption
31
What are the types of hydrocephalus?
Obstructive/non communicating | Non-obstructive/communicating: CSF is free to flow but there is an imbalance of production and absorption
32
What can cause obstructive hydrocephalus?
Tumours Congenital stenosis of the aqueduct Haemorrhage of ventricles or subarachnoid space
33
What can be seen in an obstructive hydrocephalus?
Dilation of the ventricles superior to site
34
What can cause a non-obstructive hydrocephalus?
Increased production - choroid plexus tumour | Decreased absorption - meningitis, post-haemorrhagic
35
What investigations would you request for hydrocephalus?
CT - rule out differentials | LP - opening pressure and sample CSF
36
When mustn't a lumbar puncture be carried out in a patient with a hydrocephalus?
If the cause is obstructive as the difference between pressures of the cranium and spine created by the LP will cause brain herniation
37
How does hydrocephalus present?
Signs of RICP i.e. headache worse on waking, lying down and Valsalva
38
How would hydrocephalus present in infants?
Increased head circumference - sutures not closed Anterior fontanelle bulge Sun set eye - can't look up due to superior colliculus (midbrain) compression
39
What is the triad for normal pressure hydrocephalus?
Wet wacky wobbly Urinary incontinence Dementia Disturbed gait - similar to parkinsons
40
What is a normal pressure hydrocephalus? | What is the appearance of the brain/ventricles?
Communicating hydrocephalus thought to be due to poor CSF absorption Large ventricles (particularly 4th) but normal ICP No substantial sulcal atrophy
41
What can cause a subarachnoid haemorrhage?
Traumatic or Spontaneous ``` Berry aneurysm rupture AV malformation Pituitary apoplexy Tumour invading blood vessels Idiopathic ```
42
How does a subarachnoid haemorrhage present?
``` Sudden onset thunderclap headache - occipital Vomiting Collapse, coma, seizure Meningism Terson's syndrome - vitreous haemorrhage ```
43
What are subarachnoid haemorrhages associated with?
Adult polycystic kidney disease Ehlers danlos Coarctation of the aorta
44
What can be seen on CT head in subarachnoid haemorrhages?
Hyperdense blood in: Inter-hemispheric fissure Sylvian fissues Basal cistern
45
What arteries do berry anneurysms most commonly affect?
junction of anterior cerebral and anterior communicating | junction of middle cerebral and internal carotid
46
How are subarachnoid haemorrhages managed?
Bed rest, avoid straining, maintain BP Nimodipine - 21 day to prevent vasospasm - cerebral ischaemia Surgery - endovascular coiling, craniotomy and surgical clipping
47
What complications are subarachnoid haemorrhages associated with?
Rebleeding - 20% Cerebral ischaemia - vasospasm Hydrocephalus - blockage of arachnoid granulations Hyponatraemia - SIADH
48
How would you investigate a suspected subarachnoid haemorrhage?
CT - very sensitive to timing so if suspicious do LP LP CT Angio
49
When would a lumbar puncture be carried out in suspected subarachnoid haemorrhage? What would the results be?
12 hours after headache RBC start breaking down so sample will be xanthochromic (yellow) due to bilirubin
50
What causes a subdural haemorrhage? Therefore who do they most commonly affect?
Shearing forces on cortical bridging veins | Elderly and alcoholics (brain atrophy = taught bridging veins easier to rupture)
51
How does a subdural haematoma present? Who would you see chronic subdurals in? How do they present on CT?
Slow onset of symptoms - RICP, upgoing planters etc. Chronic subdural haematomas can be seen in infants and elderly They are hypodense on CT
52
How would a subdural haematoma present on CT?
Crescent shaped hyperdense area + midline shift
53
What is the mechanism of getting an extradural haematoma? | What artery and what vein is commonly lacerated?
Acceleration Deceleration or Blow to side of head Middle meningeal artery Dural venous sinus
54
How does an extradural haematoma present?
Lucid interval followed by rapid deterioration RICP Upgoing plantars Ipsilateral pupil dilation
55
How does an extradural haematoma appear on CT?
Biconvex hyper dense area
56
What is the pathophysiology of multiple sclerosis?
Chronic cell mediated autoimmune demyelination of the CNS Attacks are separated in time and space (occur at multiple sites with remission in between)
57
What is the epidemiology of multiple sclerosis?
Mean age of onset = 30 Classically white women Combination of genetic and environmental factors
58
How does multiple sclerosis commonly present initially?
Just one symptom - e.g. pain on eye movement with blurring of vision Odd sensations such as wetness, burning or tingling
59
What systems are affected by multiple sclerosis?
``` Visual Mouth Urinary Digestive Sensory Muscular Throat - dysphagia Central ```
60
What are the visual manifestations of multiple sclerosis?
Nystagmus Optic neuritis - common first presentation Diplopia
61
What are the manifestations of multiple sclerosis seen in the mouth?
Difficulty swallowing | Slurring and stuttering of speech
62
What are the urinary manifestations of multiple sclerosis?
Frequency | Incontinence
63
What are the digestive manifestations of multiple sclerosis?
Sudden change in frequency Constipation Diarrhoea
64
What are the sensory manifestations of multiple sclerosis?
Increased sensitivity to pain Tingling Burning Pins and needles
65
What are the muscular manifestations of multiple sclerosis?
Weakness Cramping Spasm Lack of co-ordination - cerebellar involvement
66
What are the central manifestations of multiple sclerosis?
Fatigue Depression Cognitive impairment Unstable mood
67
How can multiple sclerosis progress?
3 courses: - Relapsing-remitting - complete remission between acute attacks - secondary progression - relapsing remitting over time doesn't fully remit - Primary progression - progressive deterioration from onset
68
How is multiple sclerosis diagnosed?
MRI brain - demyelination plaques MRI spine CSF Electrophoresis - oligoclonal bands of IgG Evoked potentials
69
What signs are seen in multiple sclerosis?
Lhermitte - electric shock in trunk and limb when neck flexed Uhthoff's - symptoms worse when warm Pulfrich - Unequal eye latency - straight paths appear curved
70
How is multiple sclerosis managed?
Exercise, stop smoking, avoid stress Acute relapses - IV methylprednisolone Disease modifying drugs Symtom control
71
What disease modifying drugs are used for multiple sclerosis?
Beta-interferon Glatiramer Dimethyl fumerate Alemtuzimab
72
What drugs are used in symptom management for multiple sclerosis?
Baclofen - spasticity Gabapentin - Oscillopsia and spasticity Amantidine, CBT and mindfullness - fatigue Urinary incontinence - normal meds
73
What is Parkinson's disease?
Neurodegenerative disorder of the dopaminergic neurones in the pars compacta of the substantia nigra Lewy bodies can be seen in the brainstem, cortex and basal ganglia
74
What triad of symptoms characterise Parkinson's disease?
Bradykinesia Hypertonia Tremor
75
What symptoms are associated with Parkinson's disease?
Asymmetrical symptoms Bradykinesia - slow to move, shuffling short stepped gait, micrographia, reduced arm swing, microphonia Hypertonia - leadpipe rigidity - combined with tremor = cogwheel Resting tremor - 3-5Hz, pill rolling REM sleep disorder, autonomic dysfunction, stooped posture, dementia/depression
76
What are the main differentials for Parkinson's?
``` Benign essential tremor Huntington's Wilson's Lewy body dementia Psychogenic tremor ``` Parkinson's plus - PSP, MSA, CBD
77
How is Parkinson's diagnosed?
Clinical diagnosis based on core triad + response to treatment Brain bank diagnostic criteria is used Need to rule out differentials
78
What drug classes can be used to treat Parkinsons? What important information should patients be given regarding their medication?
Don't stop abruptly and be aware of malabsorption - neuroleptic malignant syndrome Levodopa Dopamine agonists - ropinirole MAO-B Inhibitors - Rasagiline, selegiline COM-T inhibitors - entacapone
79
What needs to be given alongside Levodopa and why? What are the side effects of Levodopa?
Given with carbidopa to reduce peripheral breakdown More motor complications and more negatives: - Dyskinesia - On off effect - Dry mouth - Palpitations - Postural hypo
80
Give an example of a dopamine agonist? What effect do they have on motor symptoms and motor side effects? What are their side effects?
Ropinirole Less effect on motor symptoms but fewer motor complications Hallucinations and impulse control disorders Ergot derived (bromocriptine) last resort as cause pulmonary, retroperitoneal and cardiac fibrosis
81
Describe the use of MAO-B inhibitors in Parkinson's: Example and effect on motor symptoms/motor complications
Rasagiline Fewer motor complications but reduced effectiveness
82
What other medications are used for other symptoms of Parkinson's?
Sleepiness - Driving advice, modafinil REM sleep disorder - melatonin, clonazepam Postural hypo - fludrocortisone Hallucinations - quetiapine and lorazepam Dementia - cholinesterase inhibitor Saliva drooling - SALT, glycopyronium
83
What is the prognosis of Parkinson's and what are the main complications?
15 years Aspirational pneumonia, bed sores, infection, poor nutrition, falls, contractures
84
What is Parkinsonism?
Other conditions which appear with similar symptoms to Parkinson's but don't have same cause
85
What are the main Parkinson's plus disorders? What else can cause Parkinsonism?
Progressive supranuclear palsy Multiple system atrophy Cortico-basal degeneration Wilson's, trauma, encephalitis drugs (metoclopramide, haloperidol, chlorpromazine)
86
What symptoms would make you think a patient has progressive supra nuclear palsy?
postural instability - falling backwards symmetrical gaze palsies, speech and swallowing problems
87
What symptoms are characteristic of multiple system atrophy?
Early autonomic dysfunction - postural hypotension, urge incontinence, erectile dysfunction cerebellar signs pyramidal signs - UMN signs
88
What symptoms are associated with corticobasal degeneration?
Akinetic rigidity in 1 limb Cortical sensory loss Alien limb phenomenon apraxia: difficulty in motor planning
89
What is motor neurone disease?
Neurodegenerative disease whereby there is selective loss of upper and lower motor neurones in the motor cortex, CN nuclei and anterior horn cells NO SENSORY LOSS, no sphincter involvement or disturbance to eye movement
90
What are the types of motor neurone disease?
Amytophic lateral sclerosis - loss in motor cortex and anterior horn cells - typically UMN leg and LMN arm Primary lateral sclerosis - UMN Progressive bulbar palsy - affects brainstem motor nuclei (chewing, swallowing) Progressive muscular atrophy - LMN only typically progress from distal to proximal
91
How can motor neurone disease present?
Bulbar onset - slurred speech, swallow issues, tongue wasting UL onset - weak grip, weak abduction, hand cramp, atrophy of hand muscles LL onset - stumbling spastic gait, foot drop, thigh fasciculations, tibialis ant. wasting Resp onset - dyspnoea, aspirational pneumonia, overnight hypoventilate Frontotemporal dementia
92
How is motor neurone disease diagnosed?
Clinical diagnosis based on: - UMN and LMN signs - Disease progression No other explanation
93
How would motor neurone disease be investigated?
Normal tests to rule out differentials - LP, B12, ACh antibodies MRI - normal EMG - large amplitude but long duration (therefore less action potentials) Nerve conduction - normal motor conduction
94
What is the epidemiology of motor neurone disease?
2x more common in men 43-52 10% inherited and may present earlier
95
How is motor neurone disease managed?
MDT - palliative and end of life care Speech - SALT, aids Diet - modify diet/PEG Breathing - physio, positive pressure ventilation, BiPAP Cramps and spasms - baclofen, orthotics, exercises Drooling - Hyoscine Choking sensation - opiates Riluzole can improve survival (only by months)
96
What are the main differentials for motor neurone disease?
``` !!Cervical spondylosis!! (LMN at level and UMN below) Benign fasciculations Myasthenia gravis Inclusion body myositis Multifocal motor neuropathy Lambert-eaton ```
97
What is the prognosis for motor neurone disease?
Median survival - 2-4 years | Most die in sleep - hypercapnia
98
What is bulbar palsy?
Result of diseases affecting CN 9-12 | LMN lesions of tongue and muscles of articulation and swallowing
99
How does bulbar palsy present?
Bag of worms tongue - flaccid + fasciculations Slurred speech (R is first to go) Drooling Raspy nasal voice
100
What is pseudobulbar palsy?
Bilateral UMN lesions of corticobulbar tracts (UMN of non-ocular cranial nerves)
101
How does pseudo bulbar palsy present?
Slow tongue movements= slow deliberate speech Exaggerated jaw jerk Absent palatal movements Increased reflexes !!No wasting or fasciculations as UMN
102
What can cause bulbar and pseudo bulbar palsy?
MND Bulbar - polio, diphtheria, syringobulbia, infarct Pseudobulbar - MS, stroke
103
What is bells palsy?
Acute, unilateral, idiopathic facial nerve palsy
104
What are the risk factors for developing Bells palsy?
20-40yo Pregnancy Diabetes
105
How does bells palsy present?
``` Forehead not wrinkled Eyeballs roll up Eyelid won't close Flat nasolabial fold Paralysis of lower face Ipsilateral post-auricular numbness or pain Reduced tase Hypersensitivity to sound Can't whistle Food trapped between gum and cheek Dry eyes ```
106
What are the main differentials for bells palsy? How would you rule these out/differentiate?
Ramsay hunt - ear pain proceded by palsy. Do VSV antibodies Lyme disease - Can be bilateral. Do Borrelia antibodies Facial nerve tumour and brainstem lesions - slow onset Acoustic neuroma
107
How is bells palsy managed?
Oral prednisolone | Eye protection and lubricants
108
What complications are associated with bells palsy?
Exposure keratopathy and conjunctivitis Synkinesis - misconnected links lead to unwanted facial movements (eye blink cause upturning of mouth) Crocodile tears - cry when salivating
109
What are crocodile tears? (in reference to bells palsy)
Misconnection of parasympathetics mean unilateral lacrimation not salivation on eating
110
What is the prognosis for bells palsy?
By 6 months everyone have degree of recovery - if not consider alternate diagnosis Incomplete paralysis without axonal degeneration - recover within weeks Complete paralysis - 80% recover, 20 % start recovery later
111
What is myasthenia gravis?
Autoimmune disease where nicotinic acetylcholine receptors on the post-synaptic NMJ are blocked by antibodies
112
How does muscle fatigue progress in myasthenia gravis?
``` Extraocular Bulbar - swallow and chew Face Neck Limbs Trunk ```
113
How does myasthenia gravis present?
``` Ptosis - at night Diplopia Drooped mouth and snarl - when smiling Peek sign - eyelids separate on manual closure Voice fade on counting to 50 Unable to whistle ```
114
At what age do people commonly present with myasthenia gravis?
Women - child bearing | Men - 70's
115
What investigations are requested for Myasthenia Gravis? What are the results?
Anti-ACh antibodies Repetitive nerve stimulation shows reduced AP CT thorax - thymoma
116
What can exacerbate myasthenia gravis?
Hypokalaemia Infection Change in climate, emotion or exercise Drugs - Abx, Opiates, Beta blockers, lithium, phenytoin
117
What is myasthenia gravis associated with?
RA and SLE Thymic hyperplasia Thymic tumours
118
How is myasthenia gravis managed?
AChE inhibitors - pyridostigmine Immunosuppression - prednisolone Thymectomy Trigger avoidance
119
What are the ADR's associated with AChE inhibitors?
``` Lacrimation Salivation Sweating Vomiting Miosis ```
120
What is a myasthenic crisis?
Life threatening weakness of resp muscles
121
How can myasthenic crises be managed?
Intubate and ventilate Plasma exchange Immunosuppression and immunoglobulins
122
How could you differentiate between a myasthenic crisis and a cholinergic crisis?
Myasthenic: history of poor compliance. Good response to endrophonium challenge Cholinergic (over medicated): Other cholinergic symptoms. Endrophonium challenge leads to fasciculations, miosis and worsening respiratory function
123
What is temporal arteritis?
Granulomatous vasculitis of medium and large sized vessels Also known as giant cell arteritis
124
Who is commonly affected by temporal arteritis?
Women | >50
125
How does temporal arteritis present?
Rapid onset within <1 months Headache - temporal/occipital Jaw claudication ``` Vision changes (ant. ischaemic optic neuropathy) - amourosis fugax and visual disturbance Scalp tenderness Polymyalgia rheumatica symptoms - aching - morning stiffness (NOT WEAK) in proximal limbs Systemic symptoms - lethargic, depression, low grade fever ```
126
How would you investigate suspected temporal arteritis?
ESR - raised CRP Temporal artery biopsy - can get skip lesions so don't ignore -ve biopsy Temporal artery USS - halo sign, thickening and occlusion
127
How is temporal artery managed?
``` DONT DELAY High dose oral prednisolone - 4 weeks then taper + PPI, bisphosphonate and calcium Urgent ophthalm review Tocilizumab ``` If vision loss - IV methylprednisolone
128
What are the complications associated with temporal arteritis?
Irreversible bilateral vision loss - optic nerve ischaemia | Glucocorticoid related issues - diabetes, bone loss, infections
129
What are the types of neurofibromatosis?
Type 1 - von recklinghausen Type 2 Both autosomal dominant
130
How does neurofibromatosis type 1 present?
``` Cafe-au-lait spots (within 1st year of life and increase) Freckling Neurofibromas - dermal, nodular Lisch nodules Short Macrocephaly Mild learning disability Optic gliomas ```
131
How does neurofibromatosis type 2 present?
Cafe-au-lait spots (fewer) Bilateral vestibular schwannoma - sensorineural hearing loss, tinnitus, vertigo, compress local structures, RICP Form of cataract Meningiomas and gliomas
132
How are neurofibromatosis type 1 and 2 managed?
No cure Remove symptomatic schwannoma Annual hearing tests for type 2
133
What organisms commonly cause meningitis in adults?
Neisseria meningitidis Strep pneumoniae Listeria monocytogenes if immunocompromised
134
What investigations should be done if you suspect meningitis?
DONT DELAY TREATMENT Lumbar puncture Blood culture PCR - neisseria Blood gases
135
How would a lumbar puncture vary with the different causes for meningitis?
Bacterial - cloudy, low glucose, high protein, polymorphs Viral - clear, normal glucose and protein, lymphocytes Tuberculous - clear, low glucose, high protein, lymphocytes
136
How is meningitis managed in primary care?
Single dose benpen (ideally IV, likely IM) if non-blanching rash. If pen allergic no alternative No rash - urgent hospital transfer, no empirical abx
137
How is viral meningitis managed?
Supportive Present same as bacterial so usually follow that guidance
138
What is the general management for meningitis?
Blood cultures IV ceftriaxone - empirical Dexamethasone Meningococci - ceftriaxone Pneumococci - vancomycin + ceftriaxone HiB - ceftriaxone
139
What are the main complications associated with meningitis?
Deafness - most common Other neurological signs - epilepsy, paralysis Infections - sepsis, intracerebral abscess Pressure - brain herniation, hydrocephalus
140
What is prophylaxis is recommended for close contacts of those with meningitis?
Seek advice from regional health protection unit Usually give prophylactic abx
141
What would indicate a CT head within an hour of arrival?
``` GCS <13 GCS<15 2hrs after injury Suspected open or depressed skull fracture Signs of basal skull fracture Post-traumatic seizure Focal neurological deficit More than 1 episode of vomiting ```
142
What would indicate the C spine needs immobilisation?
``` GCS <15 Neck pain or tenderness Focal neurological deficit Paraesthesia in extremities Any clinical suspicion of cervical spine injury ```
143
What should be done is GCS <8?
Call anaesthetist
144
Why is pain management important in head injury management?
Can lead to raised ICP
145
What would indicate a CT head within 8 hours?
Patient on warfarin Some LOC or amnesia + - Age 65 years or older - Any history of bleeding or clotting disorders - Dangerous mechanism of injury - More than 30 mins retrograde amnesia of events immediately before injury
146
What is an epileptic seizure?
Transient occurrence of signs or symptoms due to abnormal electrical activity in the brain Manifest as disturbance of consciousness, behaviour, emotion, motor function or sensation
147
What is epilepsy?
Disease of brain defined by: - At least 2 unprovoked seizures more than 24hrs apart - One unprovoked seizure with risk of 2nd within 10 years similar to those who have had 2 - Diagnosis of epilepsy syndrome
148
What are the risk factors for epilepsy?
Family history Genetic condition associated - tuberous sclerosis or neurofibromatosis Febrile seizures Previous intracranial infections, brain trauma, surgery Co-morbid conditions such as CVS disease or cerebral tumours
149
How is epilepsy assessed?
``` Check for risk factors Before, during, after event EEG Imaging Bloods ``` Urgently refer all people suspected of 1st seizure
150
What general advice would you give to people with epilepsy?
``` Try and record episodes Avoid driving, swimming and bathing Protect from injury Don't restrain seizing person Place in recovery position post seizure ```
151
What is the immediate management for epilepsy?
``` >5 mins - buccal midazolam or rectal diazepam IV lorazepam if access 2 doses of drug (5 mins apart) IV phenytoin if seizures continue Intubation and Rapid sequence induction ```
152
What is the general management for epilepsy?
Monotherapy Different monotherapy Dual therapy Surgery or deep brain stimulation
153
When can anti-epileptic drug withdrawal be considered?
2-4 year seizure free Gradually withdrawn over 2-3 months
154
What is the management for generalised seizures?
1st line - Valproate 2nd line - lamotrigine or carbemazepine
155
What is the management for focal seizures?
1st - carbemazepine (or lamotrigine) 2nd - Levetiracetam or valproate
156
What are the general ADR's associated with anti-epileptic drugs?
``` Drowsiness Suicidal thoughts and behaviours Aggresion Hadaches Tremor Ataxia Gum hypertrophy Menstrual disturbance ```
157
What are the side effects of valproate and how is it monitored?
Osteoporosis, weight gain LFT for months FBC before starting
158
What are the side effects of carbamazepine and how is it monitored?
Rash, osteoporosis, SIADH, hyponatraemia, diplopia, enzyme inducer Drug conc levels, FBC, LFT, U&E, GFT monitored
159
What are the side effects of phenytoin and how is it monitored?
Rash, osteoporosis, arrhythmia, raised ALP, low Ca and folic acid, BM affected, enzyme inducer Drug conc levels and blood count monitored
160
What are the side effects of lamotrigine and how is it monitored?
Rash - inc. stephen johnsons, arrhythmia Drug conc levels
161
What are the side effects of levetiracetam and how is it monitored?
Behaviour and mood changes | Risk of infection
162
What is subacute combined degeneration of the cord?
Dorsal and lateral columns affected by vitamin B12 deficiency
163
How does subacute combined degeneration of the cord present?
Joint position and vibration sense lost Distal paraesthesia UMN signs - typically legs - extensor plantars, brisk knee reflex, absent ankle reflex
164
How is subacute combined degeneration of the cord managed and what are the complications?
Vit B12 Stiffness and weakness persist
165
What are most cerebellopontine angle tumours?
Vestibular schwannomas
166
What is a classical history of a vestibular schwannoma?
Progressive changes Vertigo Hearing loss Tinnitus Absent corneal reflex CNV, VII and VIII affected
167
How are cerebellopontine angle tumours investigated and managed?
MRI Urgent ENT referral Audiometry Observe, give radio or do surgery
168
What is the prognosis of a cerebellopontine angle tumour?
Slow growing and benign
169
What are the borders of the cavernous sinus?
Roof - meningeal layer of dura Medial - body of sphenoid Floor - endosteal layer of dura Lateral - meningeal layer of dura
170
What runs through the cavernous sinus?
``` CNIII CNIV CNV - 1 and 2 CNVI Internal carotid artery ```
171
Describe the epidemiology of a pituitary adenoma
Common - 10% of all people Often never found or found incidentally 10% of all adult brain tumours
172
How can pituitary adenomas be classified?
Size - micro <1cm macro >1cm | Hormonal status
173
What investigations are done for pituitary adenomas?
Pituitary blood profile Visual field test MRI brain with contrast Symptoms will depend on the hormones secreted and what it compresses
174
What are some differentials for pituitary adenomas?
``` Pituitary hyperplasia Craniopharyngioma Meningioma Brain mets Lymphoma Hypophysitis Vascular malformation ```
175
How are pituitary adenomas managed?
Hormone therapy Surgery - transsphenoidal transnasal hypophysectomy Radio
176
What pupil/eye changes would you see in a central herniation
fixed dilated pupils | sunset eyes - paralysed upward eye movement with pupil covered by lower lid
177
What is the contents of the cavernous sinus
Internal carotid artery CN 3,4,6 Trigeminal nerve: ophthalmic and maxillary divisions
178
What is the first line investigation for ?venous thrombosis
MRI with venography
179
Describe the passage of CSF
``` Lateral ventricle foramen of monroe 3rd ventricle cerebral aqueduct 4th ventricle foramen of luschka/magendie ```
180
How does someone with myasthenic react to different types of neuromuscular blocking anaesthetic agents?
Increased sensitivity to non-depolarising (Rocuronium) Reduced sensitivity to depolarising (Suxamethonium)