Neuro Flashcards
(150 cards)
1
Q
What is a tension type headache (TTH)?
A
A tension-type headache (TTH) is the most common type of headache and is often described as a dull, aching pain or pressure around the forehead, temples, or back of the head
2
Q
H&E of TTH
A
- Bifrontal/occipital pain
- Episodic in nature
- Pressure/band-like tightness around head
- Lasts a few hours
3
Q
RF of TTH
A
- Stress
- Fatigue
- Mental tension
4
Q
Investigations of TTH
A
First investigation is clinical diagnosis (normal neuro exam) and diagnosis via exclusion
Consider (if headache is refractory or progressing):
- CT sinus : exclude sphenoid sinusitis
- MRI : exclude brain tumour
- Lumbar puncture : exclude infective causes, sinus venous thrombosis or pseudotumour cerebri
5
Q
Management of TTH
A
Acute - simple analgesics (aspirin, paracetamol, ibuprofen or naproxen)
Chronic (> 7-9/month)
- antidepressant (amitriptyline or doxepin)
- muscle relaxant (tizanidine)
- consider non-drug therapies
Prophylactic acupuncture
6
Q
What is a Stroke?
A
- AKA Cerebrovascular Accident
- Represents a sudden interruption in the vascular supply of the brain
- Two types are haemorrhagic and ischaemic
7
Q
H&E for Stroke
A
- motor weakness
- dysphagia
- swallowing problems
- homonymous hemianopia
- balance problems
Cerebral Hemisphere infarcts
- contralateral hemiplegia
- contralateral sensory loss
- homonymous hemianopia
- dysphasia
Brainstem infarct
- More severe symptoms including quadriplegia and lock-in syndrome
Lacunar infarct
- small infarcts around basal ganglia, internal capsule, thalamus and pons
- may result in pure motor, pure sensory, mixed signs or ataxia
7
Q
What is Subdural Haemorrhage?
A
A collection of blood deep to the dural layer of the meninges
Blood is not within the substance of the brain and therefore is called an ‘extra-axial’ or ‘extrinsic’ lesion
Can be uni- or bi-lateral
8
Q
How can Subdural Haemorrhage be classified?
A
Acute - most commonly caused by high-impact trauma, often underlying brain damage
Subacute
Chronic - present for weeks to month, rupture of the small bridging veins within subdural space that cause slow bleeding
Elderly and alcoholic patients are at risk since they have brain atrophy and therefore fragile and taut bridging veins
9
Q
H&E of Subdural Haemorrhage
A
Key
- Headache
- Evidence of trauma
- N + V
- Low GCS
- Confusion
Other
- Loss of consciousness
- Seizure
- Loss of continence
- Focal neurological deficits
10
Q
RF for Subdural Haemorrhage
A
- Recent trauma
- Anticoagulant use
- Alcoholism
- Advanced age
11
Q
Investigations for Subdural Haemorrhage
A
1st
- Non-contrast CT head
- Shows fluid collection
- Crescenteric collection, not limited by suture lines
- Acute bleeds appear hyper dense, whereas chronic is hypo dense
- Large acute haematomas will cause ‘mass effect’ - midline shift or herniation
12
Q
Management of Acute Subdural Haemorrhage
A
- If <10mm, <5mm midline shift and non-expansile without neurological dysfunction - conservative management
- If >10mm, >5mm midline shift, expansile, or neurological dysfunction - craniotomy
Antiepileptics if seizures/risk of seizures (phenytoin/levetiracetam)
13
Q
Management of Chronic Subdural Haemorrhage
A
- Manage conservatively if small and no neurological deficit
- If patient is confused, has neurological deficit or severe image findings - surgical decompression with burr holes
Antiepileptics if seizures/risk of seizures (phenytoin/levetiracetam)
14
Q
What is spinal cord compression?
A
An oncological emergency and effects up to 5% of cancer patients
Extradural compression accounts for majority of cases, usually due to vertebral body mets
More common in patients with lung, breast and prostate cancer
15
Q
H&E of Spinal Cord Compression
A
- back pain - earliest and most common symptom, may be worse when prone or coughing
- lower limb weakness
- sensory changes : loss and numbness
- neurological signs dependent on level of lesion
- above L1 usually UMN signs in legs and a sensory level
- below L1 usually LMN signs in legs and perianal numbness
- tendon reflexes tend to be increased below level of lesion and absent at level of lesion
16
Q
Investigations for Spinal Cord Compression
A
- Urgent whole spine MRI within 24hrs of presentation
17
Q
Management of Spinal Cord Compression
A
- high dose oral dexamethasone
- urgent oncological assessment for consideration or radiotherapy or surgery
18
Q
What is Bell’s palsy?
A
- Type of facial paralysis that occurs due to the dysfunction of the facial nerve, usually due to inflammation or compression
- MC cause of acute facial weakness
- Can occur at any age but is more common between 15-60 years old
19
Q
H&E of Bell’s palsy
A
- May present with sudden onset facial weakness or paralysis, usually unilateral
- Drooping of mouth, inability to close the eye on the affected side, drooping of eyelid and altered taste sensation may present
- Exam may reveal weakness or paralysis of muscle of facial expression as well as loss of corneal reflex and hyperacusis
20
Q
Investigations of Bell’s palsy
A
- First-line is thorough history and exam to rule out other causes of facial nerve dysfunction
- If diagnosis uncertain, further investigations such as EMG or imaging such as MRI or CT
21
Q
Management of Bell’s palsy
A
- Corticosteroid therapy, initiated ASAP from onset of symptoms
- High dose (50-60mg) prednisolone within 72 hours
- Prednisolone 25mg orally once daily for 10 days for most patients
- Antiviral therapy may also be considered in some cases if there is evidence of HSV
- Eye care is essential to prevent corneal damage - artificial tears, ointments and eye patches
- PT and facial exercises may be beneficial
- Most patients recover in 3-6 months, although some may experience persistent or recurrent symptoms
22
Q
What is Myasthenia Gravis?
A
An autoimmune disorder resulting in insufficient functioning acetylcholine receptors
Antibodies to Ach receptors seen in 85-90% of cases
F>M
23
Q
Exacerbating factors of Myasthenia Gravis
A
MC factor is exertion resulting in fatiguability - hallmark feature
Exacerbating drugs:
- Penicillamine
- Quinidine, procainamide
- BBs
- Lithium
- Phenytoin
- Abx : gentamicin, macrolides, quinolones, tetracyclines
24
H&E of Myasthenia Gravis
Key feature is muscle fatiguability - muscles become progressively weaker during rest periods of activity and slowly improve after rest
- Extraocular muscles : diplopia
- Proximal muscle weakness : face, neck, limb girdle
- Ptosis
- Dysphagia
Associated with :
- Thymomas in 15%
- Autoimmune conditions : pernicious anaemia, thyroid, rheumatoid, SLE
- Thymic hyperplasia in 50-70%
25
Investigations for Myasthenia Gravis
- Antibodies to Ach Receptors
- +ve in 85-90%
- in remaining patients, 40% positive for anti-muscle-specific tyrosine kinase antibodies
- antibodies are less commonly seen in disease limited to ocular muscles
- CK normal
- CT thorax to exclude thymoma
- single fibre EMG : high sensitivity (92-100%)
26
Management on Myasthenia Gravis
- Pyridostigmine (long-acting Ach-erase inhibitor)
- Immunosuppression is usually not started at diagnosis but majority of patient will end up needing it
- Prednisolone initially
- Azathioprine, cyclosporine, mycophenolate, mofetil may also be used
- Thymectomy
27
Management of Myasthenia Gravis Crisis
- Plasmapheresis
- IV Immunoglobulins
28
What is Trigeminal Neuralgia?
A type of chronic pain disorder that involves sudden attacks of severe facial pain
Occurs more often in women
Typical age of onset is 60-70yo
29
H&E for Trigeminal Neuralgia
- Unilateral stabbing, sharp facial pain
- Involving one or more division of trigeminal nerve
- Lasts seconds
- Triggered by eating, laughing, talking or touching affected area
30
RF for Trigeminal Neuralgia
- Increasing age
- Female
- MS
31
Investigations for Trigeminal Neuralgia
Clinical diagnosis
Other investigations to consider:
- Intra-oral XR - if dental cause suspected
- MRI - if other pathology suggested
- Trigeminal reflex testing - after diagnosis, early blink reflex or early masseter inhibitory reflex
32
Management of Trigeminal Neuralgia
- Anticonvulsant - carbemazepine
- Refer to neurology if failure to respond to treatment or atypical features
33
Red Flags for Trigeminal Neuralgia
- Sensory changes
- Deafness or other ear problems
- Hx of skin or oral lesions that could be spread perineurally
- Pain only in opthalmic division or bilaterally
- Optic neuritis
- FHx of MS
- Age of onset before 40yo
34
What is Wernicke’s Encephalopathy?
Neuropsychiatric disorder caused by thiamine deficiency, MC seen in alcoholics
Rarer causes include persistent vomiting, stomach cancer and dietary deficiency
Classic triad of opthalmoplegia/nystagmus, ataxia and encephalopathy may occur
Petechial haemorrhages occur in variety of structures in brain including mamillary bodies and ventricle walls
35
H&E of Wernicke’s Encephalopathy
Occulomotor dysfunction
- nystagmus
- opthalmoplegia (lateral rectus palsy, conjugate gaze palsy)
Gait ataxia
Encephalopathy (confusion, disorientation, indifference, inattentiveness)
Peripheral sensory neuropathy
36
Investigations of Wernicke’s Encephalopathy
- Decreased red cell transketolase
- MRI : areas of symmetrical inc. T2/FLAIR signal
37
Management of Wernicke’s Encephalopathy
Treatment is with urgent replacement of Thiamine
- Give Pabrinex (IV B/C vitamins) : replaces thiamine and prevents the condition from progressing to Korsakoff’s psychosis
38
What is Korsakoff’s Syndrome?
If Wernicke’s Encephalopathy not treated, Korsakoff's syndrome may develop as well. This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation (generation of false memories) in addition to the above symptoms.
39
What is Chronic Fatigue Syndrome?
Diagnosed after 3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms
MC in women
Past psychiatric Hx has not been shown to increase risk
40
H&E of Chronic Fatigue Syndrome
- Fatigue is central feature
- Sleep problems
- Muscle or joint pains
- Headaches
- Painful lymph nodes without enlargement
- Sore throat
- Cognitive dysfunction (brain fog e.g.)
- Physical or mental exertion
- General malaise
- Dizziness
- Nausea
- Palpitations
41
Investigations for Chronic Fatigue Syndrome
DO ALL TEST TO EXCLUDE OTHER PATHOLOGY
e.g. bloods, coeliac screening, urinalysis, hormones
42
Management of Chronic Fatigue Syndrome
- Refer to specialist CFS service
- Energy management
- Physical activity and exercise overseen by specialist
- Cognitive behavioural therapy
43
Causes of Brain Abscess
- Extension of sepsis from middle ear or sinuses
- Trauma or surgery to the scalp
- Penetrating head injuries
- Embolic events from endocarditis
44
H&E of Brain Abscess
Presenting symptoms depend upon site of abscess, considerable mass effect to due raised ICP
- Headache : often dull and persistent
- Fever : may be absent and usually not the swinging pyrexia seen with abscess in other sites
- Focal neurology : site or due to inc. ICP
- Nausea, papilloedema, seizure : inc. ICP
45
Investigations for Brain Abscess
Imaging : CT scanning
46
Management of Brain Abscess
Surgery: craniotomy to relieve inc. ICP + abscess debridement but it may reform because head is closed following drainage
IV Abx: IV 3rd-gen cephalosporin + metronidazole
ICP management: e.g. dexamethasone
47
MC cancer that metastasise into the brain
- Lung (MC)
- Breast
- Bowel
- Skin (namely melanoma)
- Kidney
48
Management of Brain Mets
- Radiation
- Chemotherapy
- Immunotherapy
- Supportive Care
49
What causes Diabetic Neuropathy?
Caused by blockage of vasa nervorum due to increased blood glucose concentration
50
Features of Peripheral Diabetic Neuropathy
Glove and stocking distribution
Loss of sensation, particularly in feet
May not sense injury, so important to inspect feet
Neuropathic ulcer typically develop over callouses or pressure points
Loss of ankle jerk/ vibration sense/ fractures (Charcot’s joint)
51
Features of Diabetic Mononeuropathy
- Sudden motor loss
e.g. Wrist drop, foot drop, 3rd nerve palsy
52
Features of Autonomic Diabetic Neuropathy
GI tract - difficulty swallowing, delayed gastric emptying, bladder dysfunction
Postural hypotension
Cardiac autonomic supply
53
Management of Diabetic Neuropathy
- Glycaemic control
- Neuropathic pain agent : duloxetine, amitriptyline, pregabalin, gabapentin
- Tramadol as rescue therapy for exacerbations
- Topical capsaicin for localised neuropathic pain
- Pain management clinics for resistant problems
54
What is Essential Tremor?
An autosomal dominant condition which usually affects both upper limbs
55
Signs + Symptoms of Essential Tremor
Postural tremor: worse when arms outstretched
Improved by alcohol and rest
MC cause of titubation (head tremor)
56
Management of Essential Tremor
- Propranolol is first-line
- Primidone is sometimes used
57
What is MND?
Neurological condition of unknown cause which can present with both UMN + LMN signs
Rarely presents before 40 years of age
58
Features of Amyotrophic Lateral Sclerosis
- 50% of patients
- Typically LMN signs in arms and UMN signs in legs
- In familial cases, the gene responsible lies on chromosome 21 and codes for superoxide dismutase
- Asymmetric limb weakness
- Mix of UMN and LMN signs
- Wasting of small hand muscles/ tibialis anterior
- Fasciculations
- Absence of sensory signs/ symptoms
59
Features of Primary Lateral Sclerosis
UMN signs only
60
Features of Progressive Muscular Atrophy
LMN signs only
Affects distal muscles before proximal
Carries best prognosis
61
Features of Progressive Bulbar Palsy
- Palsy of tongue, muscles of chewing/ swallowing and facial muscles due to loss of function of brainstem motor nuclei
- Carries worst prognosis
- Dysarthria
- Dysphagia
- Wasted fasciculating tongue
- Brisk jaw jerk reflex
62
Other features of MND
DOESN’T affect external ocular muscles
No cerebellar signs
Preserved abdominal reflexes
Sphincter dysfunction is a late sign
63
Investigations of MND
Clinical diagnosis
Nerve conduction studies show normal conduction
Electromyography - reduced AP with inc. amplitude
MRI to exclude cervical cord compression and myelopathy
64
Management of MND
Riluzole - usually in ALS
NIV (BiPaP at night
Percutaneous gastrostomy tube for nutrition
65
What is Normal ICP and what is CCP?
Normal ICP is 7-15 mmHg in supine adults
CCP is cerebral perfusion pressure : net pressure gradient causing cerebral blood flow to brain = MAP - ICP
66
Causes of Raised ICP
- Space-occupying lesion
- Cerebral oedema
- Inc. blood pressure in CNS
- Hydrocephalus
67
H&E of Raised ICP
Key:
- Headache often worse when lying down
- N+V usually in the morning
- Papilloedema
- Cushing’s triad: widening pulse pressure, bradycardia, irregular breathing
Other:
- Reduced levels of consciousness
- Cushing’s peptic ulcer: epigastric pain
68
Investigations of Raised ICP
CT/ MRI
Invasive ICP monitoring:
- catheter placed in lateral ventricles
- can take CSF samples and drain small amounts
- cut-off of >20 mmHg determines need for further treatment
69
Management of Raised ICP
Treat underlying cause
Head elevation to 30 degrees
IV mannitol - osmotic diuretic
Controlled HT - reduce pCO2 = vasoconstriction of cerebral arteries = reduced ICP
Removal of CSF - drain from intraventricular monitor, repeated lumbar puncture (idiopathic intracranial HT), ventriculoperitoneal shunt (hydrocephalus)
70
Features of Radial Nerve Palsy
Wrist drop
Sensory loss to small area between dorsal aspect of 1st and 2nd metacarpals
71
Features of Radial Nerve Palsy
Wrist drop
Sensory loss to small area between dorsal aspect of 1st and 2nd metacarpals
Paralysis of Triceps
72
Features of Common Peroneal Nerve Palsy
Injury often occurs at neck of fibula
MC characteristic is foot drop
Also:
- weakness of foot dorsiflexion
- weakness of foot eversion
- weakness of extensor hallucis longus
- sensory loss over dorsum of foot and lower lateral part of leg
- wasting of anterior tibial and peroneal muscles
73
Features of Ulnar Nerve Palsy at Wrist
- 'claw hand' - hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
- wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
- wasting and paralysis of hypothenar muscles
- sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)
74
Features of Ulnar Nerve Palsy at Wrist
- 'claw hand' - hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
- wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
- wasting and paralysis of hypothenar muscles
- sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)
75
Features of Ulnar Nerve Palsy at Elbow
- 'claw hand' - hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
- wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
- wasting and paralysis of hypothenar muscles
- sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)
- clawing is more severe at elbow
- radial deviation of wrist
76
Features of Median Nerve Palsy at Elbow
- pain/pins and needles in thumb, index, middle finger
- unusually the symptoms may 'ascend' proximally
- patient shakes his hand to obtain relief, classically at night
- weakness of thumb abduction (abductor pollicis brevis)
- wasting of thenar eminence (NOT hypothenar)
- Tinel's sign: tapping causes paraesthesia
- Phalen's sign: flexion of wrist causes symptoms
ALSO
- Loss of forearm pronation
- Weak wrist flexion
- Ulnar deviation of wrist
77
Features of Damage to Anterior Interosseus Nerve
- Loss of forearm pronation
- Weakness of long flexors of thumb and index finger
78
What is Carpal Tunnel Syndrome?
Caused by compression to medial nerve at wrist in the carpal tunnel
79
H&E of Carpal Tunnel Syndrome
History
- pain/pins and needles in thumb, index, middle finger
- unusually the symptoms may 'ascend' proximally
- patient shakes his hand to obtain relief, classically at night
Examination
- weakness of thumb abduction (abductor pollicis brevis)
- wasting of thenar eminence (NOT hypothenar)
- Tinel's sign: tapping causes paraesthesia
- Phalen's sign: flexion of wrist causes symptoms
80
Causes of Carpal Tunnel Syndrome
- Idiopathic
- Pregnancy
- Oedema e.g. HF
- Lunate fracture
- Rheumatoid arthritis
81
Findings of Electrophysiology for Carpal Tunnel Syndrome
Motor + sensory: prolongation of AP
82
Treatment of Carpal Tunnel Syndrome
NICE Clinical Knowledge Summaries currently recommends a 6-week trial of conservative treatments if the symptoms are mild-moderate
- corticosteroid injection
- wrist splints at night
If there are severe symptoms or symptoms persist with conservative management:
- surgical decompression (flexor retinaculum division)
83
What is a Radiculopathy?
Injury or damage to nerve roots in the area where they leave the spine
84
What does L5 radiculopathy cause?
Foot drop and weakness of hip abduction
85
Pathophysiology of Encephalitis
- HSV-1 is responsible for 95% of adult cases
- Typically affects temporal and inferior frontal lobes
86
H&E of Encephalitis
- Fever
- Headache
- Psychiatric symptoms
- Seizures
- N+V
- Focal feature e.g. aphasia
- Peripheral lesions have no relation to the presence of HSV Encephalitis
87
Investigations for Encephalitis
CSF
- Lymphocytosis
- Elevated proteins
- PCR for HSV, VZV and enteroviruses
MRI
- medial temporal and inferior frontal changes e.g. petechial haemorrhages
- normal in 1/3 patients
EEG
- lateralised periodic discharges at 2 Hz
88
Management of Encephalitis
IV aciclovir should be started in all cases of suspected encephalitis
89
Mechanism and Side effects of Lamotrigine
Sodium channel blocker
Can lead to Steven Johnson syndrome
90
Mechanism and Side Effects of Sodium Valproate
Sodium channel blocker
Teratogenic - leads to neural tube defects
91
Side Effects of SSRIs and TCAs
Known to cause prolonged QT syndrome in some patients
Particularly seen with citalopram - can lead to Torsades de Pointes
92
Side Effects of Phenytoin
Used in management of seizures
Can cause megaloblastic anaemia by altering metabolism of folate
93
Common adverse effects of Levadopa
- Dry mouth
- Anorexia
- Palpitations
- Postural hypotension
- Psychosis
94
Adverse effects of Levadopa due to unsteady dose
- End-of-dose wearing off: symptoms often worsen towards end of dosage interval - decline of motor activity
- On-off phenomenon: large variations in motor performance with normal function during the on period and restricted mobility in off period
- Dyskinesias at peak dose: dystonia, chorea + athetosis
- Worsen over time - clinician therefore may limit doses until necessary
95
What is MS?
Chronic cell-mediated autoimmune disorder characterised by demyelination in the CNS
96
Epidemiology of MS
- F > M
- MC diagnosed aged 20-40
- Much more common at higher latitudes (5x more common than in tropics)
97
What is Relapsing-remitting MS?
MC form of MS, 85% of patients
Acute attacks (e.g. 1-2months) followed by periods of remission
98
What is Secondary progressive MS?
Similar to RR MS but the deteriorate between periods of remission
65% of RR MS patients develop this
Gait and bladder disorder are generally seen
99
What is Primary progressive MS?
10% of patients
Progressive deterioration from onset that is continuous
MC in older people
100
H&E of MS
- Lethargy
- Optic neuritis
- Optic atrophy
- Uhthoff’s phenomenon : worsening of vision following rise of body temp
- Paraesthesia
- Lhermitte’s syndrome : paraesthesia in limbs on neck flexion
- Spastic weakness
- Ataxia during acute relapse
- Tremor
- Urinary incontinence, sexual dysfunction and intellectual deterioration
101
Investigations for MS
Dissemination in space and time
MRI - high signal T2 lesions, periventricular plaques, Dawson fingers (in FLAIR images) - hyper intense lesions perpendicular to corpus callosum
Lumbar puncture - oligoclonal bands in CSF (not in serum), increased intrathecal synthesis of IgG
Visual evoked potentials - delayed but well preserved waveform
102
Management of MS
Treatment is focused on reducing frequency and duration of relapses - no cure
103
Acute relapse management of MS
High dose steroids (shortens length of relapse)
Methylprednisolone
104
Reducing risk of relapse management of MS
If RR or 2nd-P and 2 relapses in last 2 years
IV Natalizumab
IV Ocrelizumab
105
Managing fatigue in MS
Amantadine (after excluding other causes)
CBT, mindfulness training
106
Management of Spasticity in MS
- Baclofen and gabapentin
- PT and OT
107
Management of Bladder dysfunction in MS
- US to assess bladder emptying
- If significant residual volume - intermittent self-catheterisation
- If not - anticholinergics may improve urinary frequency
108
Management of Oscillopsia in MS
Gabapentin
109
What is Meningitis?
Inflammation of the leptomeninges and the cerebrospinal fluid of the subarachnoid space
110
What is Viral Meningitis?
Inflammation attributed to a viral agent.
In comparison to bacterial, it may be considered to be more benign and is much MORE COMMON
111
Causes of VIral Meningitis
- Non-polio enteroviruses e.g. Coxsackie Virus, Echovirus
- Mumps
- Herpes Simplex Virus (HSV), Cytomegalovirus (CMV), Herpes Zoster Virus
- HIV
- Measles
112
RF for Viral Meningitis
- Patients at extremes of ages (<5 and the elderly)
- Immunocompromised (e.g. renal failure or diabetes)
- IVDU
113
Causes of Bacterial Meningitis
Group B Streptococcus is most common in neonates
Neisseria Meningitides causes Meningococcal disease, most common in children
Streptococcus pneumoniae and Haemophilus Influenzae can also cause it in kids
Enteroviruses is the most common cause of meningitis in adults (e.g. Coxsackie B virus)
114
H&E of Meningitis
Common :
- Headache
- Neck stiffness
- Photophobia
- Confusion
(DUE TO FLUID BUILD UP)
- Fevers
Less common :
- Focal neurological deficits on exam
- Seizures : suggests a meningoencephalitis = raised ICP
115
Special signs of Meningitis
Purpuric rash particularly in invasive meningococcal disease due to toxins damaging blood vessels
Brudzinski Sign - passive flexion of neck = flexion of knee
Kernig Sign - passive flexion of knee then slowly extending = resistance, pain or inability to extend
Fundoscopy to look for papilloedema = raised ICP
116
Investigations for Meningitis
Lumbar Puncture
Contraindicated or delayed :
- Signs of severe sepsis or radially evolving rash
- Severe respiratory/cardiac compromise
- Significant bleeding risk
- Signs of raised ICP = focal signs, papilloedema, seizures, GCS<12
- PCR
117
CSF findings for Bacterial Meningitis
- Cloudy appearance
- Glucose LOW (< 1/2 plasma)
- Protein HIGH (> 1 g/l)
- White cells 10-5000 polymorphs/mm3 (Neutrophils)
118
CSF findings for Viral Meningitis
- Clear/cloudy appearance
- 60-80% of plasma glucose
- Normal/raised protein
- 15-1000 lymphocytes/mm3
119
CSF findings for Tuberculous Meningitis
- Slight cloudy/ fibrin web
- Low glucose (<1/2 plasma glucose)
- High protein (> 1g/l)
- 30-300 lymphocytes/mm3
120
CSF finding for Fungal Meningitis
- Cloudy appearance
- Low glucose
- High proteins
- 20-200 lymphocytes/mm3
121
Management of Viral Meningitis
- Supportive care
- Self-limiting
- Ceftriaxone and aciclovir if suspecting bacterial or encephalitis
- Aciclovir if secondary to HSV
122
Management of Bacterial Meningitis
- Urgent hospital admission
- If in primary care + suspecting meningococcal give IM benzylpenicillin
- ABCDE approach
- LP if able
- IV Abx
- IV dexamethasone (not in meningococcal septicaemia, recent surgery, septic shock or immunocompromised)
123
Abx used for treatment of Bacterial Meningitis
<3 months old : IV cefotaxime + amoxicillin
3 months - 50 years olds : IV cefotaxime
> 50 years old : IV cefotaxime + amoxicillin
Meningococcal : IV benzylpenicillin or cefotaxime
124
Management of Meningitis if raised ICP
- Get critical care input
- Secure airway + high-flow oxygen
- IV access : bloods and cultures
- IV dexamethasone
- IV Abx
- Arrange neuroimaging
125
Management of Meningitis if severe sepsis/ rapidly evolving rash
- Get critical care input
- Secure airway + high-flow oxygen
- IV access : blood + cultures
- IV fluid resus
- IV Abx
126
Prophylactic treatment for contacts of patients with Meningococcal meningitis
Oral ciprofloxacin or rifampicin
127
Complications of Meningitis
- Sensorineural hearing loss : MC
- Seizures
- Focal deficits
- Sepsis
- Intracerebral abscess
- Brain herniation
- Hydrocephalus
Patients w/ meningococcal at risk of Waterhouse-Freidrichsen syndrome (adrenal insufficiency secondary to adrenal haemorrhage)
128
International League Against Epilepsy (ILAE) criteria
1. At least 2 unprovoked (or reflex) seizures occurring greater than 24 hours apart
2. One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
3. Diagnosis of an epilepsy syndrome - epilepsy is considered to be resolved for individuals who had an age-dependent epilepsy syndrome but are now past the applicable age or those who have remained seizure-free for the last 10 years, with no seizure medicines for the last 5 years.
129
Basic Classification of Epilepsy
1. Where seizures begin in the brain
2. Level of awareness during a seizure
3. Other features of seizures
130
H&E of Generalised Tonic-Clonic
Loss of consciousness, stiffening and jerking of the body
Patients who have had generalised seizures may
- bite their tongue
- experience incontinence of urine
Following seizure, patients typically have a postictal phase where they are drowsy and tired for around 15 mins
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H&E of Focal Seizure
- Frontal lobe : motor abnormalities and Jacksonian movements
- Parietal lobe : sensory abnormalities
- Temporal lobe : automatisms (plucking of clothes, smacking lips, grabbing), aura (rising epigastric sensation, deja-vu, hallucinations)
- Occipital lobe : floaters/flashes
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H&E of Myoclonic Seizures
- Bilateral upper and lower limb contracting and relaxing (clonus)
- No loss of consciousness, incontinence, tongue-biting, or a postictal phase characterised by fatigue
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H&E of Absence Seizures
- Episodes of staring blankly into space and being unresponsive
- Typically seen 3-10yo, most become seizure free by adolescence
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H&E of Atonic Seizures
Sudden weakness in all body muscles, short duration and retained awareness
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What is Juvenile Myoclonic Epilepsy?
Genetic generalised epilepsy syndrome including absence, myoclonic and generalised tonic-clonic seizures
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Investigations for Epilepsy
- EEG : absence seizures : 3Hz spike and wave
- MRI
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What is Status Epilepticus?
- single seizure lasting > 5 mins, or
- >/ 2 seizures within a 5 min period without the person returning to normal between them
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Management of Status Epilepticus
ABC
- airway adjunct
- oxygen
- check blood glucose
IV benzodiazepines e.g. diazepam or lorazepam
- pre-hospital : PR diazepam or buccal midazolam
- in hospital IV lorazepam (can be repeated after 10-20mins)
- second line phenytoin or phenobarbital
- GA if longer than 45 mins
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Management of Generalised Tonic-Clonic Seizures
Males : sodium valproate
Females : lamotrigine or levetiracetam
Girls < 10yo may be offered sodium valproate first-line
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Management of Focal Seizures
First-line : lamotrigine or levetiracetam
Second-line : carbemazepine, oxcarbazepine or zonisamide
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Management of Absence Seizures
First-line : ethosuximide
Second-line :
- Male : sodium valproate
- Female : lamotrigine or levetiracetam
CARBAMAZEPINE MAY EXACERBATE
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Management of Myoclonic Seizures
Males : sodium valproate
Female : Levetiracetam
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Management of Tonic or Atonic Seizures
Males : sodium valproate
Females : lamotrigine
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Cause of Sub-arachnoid Haemorrhage
MOST COMMON : traumatic SAH
- Intracranial aneurysm (saccular berry aneurysm) 85% : APCKD, Euler-Danlos syndrome and coarctation of aorta
- AV malformation
- Pituitary apoplexy
- Arterial dissection
- Mycotic (infective) aneurysms
- Perimesencephalic (idiopathic venous bleeding)
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H&E of Sub-arachnoid Haemorrhage
Key :
- Severe sudden-onset ‘thunderclap’ headache
- Depressed/ loss of consciousness
- Neck stiffness and muscle aches
Other :
- Photophobia
- N+V
- Confusion
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RF for Sub-arachnoid Haemorrhage
HT
Smoking
FHx
APCKD
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Investigations of Sub-arachnoid Haemorrhage
Non-Contrast CT : hyper density within basal cisterns and sulci of SA space
ECG
Bloods : FBC - leukocytosis, U&Es - SIADH, Clotting profile, Troponin, Serum glucose may be elevated
Other :
- LP if CT head is -ve - at least 12 hours after onset of symptoms to allow development of xanthochromia
- CT angiography - when SAH confirmed
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Management of Sub-arachnoid Haemorrhage
- Cardiopulmonary support
- Prothrombin complex concentrate, IV vit K to reverse warfarin effect
- Platinum coil for intracranial aneurysm - consider craniotomy and clipping
- Nimodipine to prevent vasospasm
- Treat hydrocephalus with external ventricular drain or long-term ventriculoperitoneal shunt
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Complications of Sub-arachnoid Haemorrhage
Re-bleeding : (10%) and MC in first 12 hours, if suspected repeat CT
Vasospasm typically 7-14 days after
Hyponatraemia - SIADH
Seizures
Hydrocephalus
Death
