Week 3 Flashcards
1
Q
what are the names of 3 common cognitive screens?
A
- mini mental state examination (MMSE)
- montreal cognitive assessment (MOCA)
- addenbrooke’s cognitive examination (ACE-III)
2
Q
what are the ‘special’ senses and which cranial nerves allow these?
A
- olfaction (I)
- vision (II)
- taste (VII, IX and X)
- hearing and balance (VIII)
3
Q
which cranial nerves are involved with ‘ordinary’ sensation?
A
- mainly the Vth (trigeminal nerve).
- the ear from the facial (VII) and (glossopharyngeal (IX) nerves.
4
Q
the eye muscles are controlled by which cranial nerves?
A
- oculomotor III
- trochlear IV
- abducens VI
5
Q
the muscles of mastication are controlled by which cranial nerve?
A
V (trigeminal)
6
Q
the muscles of facial expression are controlled by which cranial nerve?
A
facial VII
7
Q
the muscles of the larynx and pharynx are controlled by which cranial nerves?
A
mainly vagus (X) but also glossopharyngeal
8
Q
which cranial nerve controls movement of the SCM and trapezius muscles?
A
accessory (XI)
9
Q
which cranial nerves have autonomic functions (all parasympathetic) and what are the functions?
A
- oculomotor III > pupillary constriction.
- facial VII > lacrimation.
- facial VII > salivation from submandibular and sublingual glands.
- glossopharyngeal IX > salivation from parotid gland.
- vagal X input to organs in thorax and abdomen.
10
Q
how do we test the function of the optic nerve II?
A
- visual acuity
- visual fields
- pupillary reactions
- fundoscopy
- colour vision
11
Q
how do we test the function of the oculomotor, trochlear and abducens cranial nerves?
A
- any evidence of ptosis?
- pupil of equal size?
- pupillar reactions.
- eye movements > vertical and horizontal.
12
Q
how do we test the function of the trigeminal nerve?
A
- sensation in the opthalamic, maxillary and mandibular regions with e.g. cotton wool.
- power in muscles of mastication.
- corneal reflex.
- jaw jerk.
13
Q
how do we test the function of the facial nerve?
A
- test muscles of facial expression.
- corneal reflex.
- taste.
14
Q
how do we test the vestibulocochlear nerve function?
A
- hearing using Rinne’s and Weber’s tests.
- vestibular function using Dix-Hallpike maneouvre and Utenberger’s test.
15
Q
how do we test the function of the glossopharyngeal and vagal nerves?
A
- movement of the palate
- gag reflex
- quality of speech
- quality of cough
16
Q
how do we test the function of the accessory nerve XI?
A
- head turning and shoulder shrugging.
17
Q
how do we test th function of the hypoglossal nerve?
A
appearance, movement and power of tongue
18
Q
what is the location of the oculomotor and trochlear cranial nerve nuclei?
A
mid brain
19
Q
what is the location of the trigeminal, abducens and facial cranial nerve nuclei?
A
pons
20
Q
what is the location of the vestibulocochlear cranial nerve nuclei?
A
pontomedullary junction
21
Q
what is the location of the glossopharyngeal, vagus, accessory and hypoglossal nerve nuclei?
A
medulla
22
Q
what causes optic neuritis?
A
- demyelination within the optic nerve.
- often associated with multiple sclerosis.
23
Q
what are the consequences of optic neuritis?
A
- monocular visual loss
- pain on eye movement
- reduced visual acuity
- reduced colour vision
- optic disc may be swollen
24
Q
what are some causes of an isolated third nerve palsy?
A
microvascular causes (painless, pupil spared):
- diabetes
- hypertension
compressive causes (painfule, pupil affected):
- posterior communicating artery aneurysm
- raised ICP
25
what are some causes of an isolated sixth nerve palsy?
- idiopathic
- diabetes
- meningitis
- raised ICP
26
what causes trigeminal neuralgia?
- caused by compression of trigeminal nerve in the posterior fossa.
27
what is the first-line treatment for trigeminal neuralgia?
carbamazepine
28
what is dysarthria?
disordered articulation
slurring of speech
29
what causes pseudobulbular palsy?
- bilateral UMN lesions of CN IX-XII
- site > internal capsule
- MND, MS
30
what causes a bulbar palsy?
- bilateral LMN lesions affecting IX-XII
- site > medulla
- MND, polio, tumours, vascular lesions of the medulla, syphilis.
31
what are symptoms and signs of bulbar palsy?
- absent/reduced gag reflex
- wasted, fasciculating tongue
- jaw jerk absent/normal
- dysarthria (nasal)
- dysphagia
32
what are symptoms and signs of pseudobulbar palsy?
- exaggerated gag reflex
- spastic tongue
- jaw jerk increased
- spastic dysarthria
- emotional lability
33
how would you describe a functional neurological disorder?
change in function rather than structure of a system (blackouts, paralysis, abnormal movements).
34
what is Hoover's sign when assessing functional symptoms and signs in neurology?
35
meningitis definition
- inflammation/infection of meninges.
36
encephalitis definition
inflammation/infection of brain substance
37
myelitis definition
inflammation/infection of spinal cord
38
signs and symptoms of meningitis
- headache
- fever
- neck stiffness
- photophobia
- nausea and vomiting
- focal neurology
- seizures
- reduces conscious level
- non-blanching petechial rash indicative of sepsis
39
what test is used to look for a petechial skin rash in meningitis?
Tumbler test
40
what are the organisms responsible for bacterial meningitis?
- Neisseria meningitidis (meningococcus).
- Streptococcus pneumoniae (pneumococcus).
41
what type of virus can cause meningitis?
enteroviruses
42
what are the signs and symptoms of encephalitis?
- fever
- flu-like prodromal illness (4-10 days)
- seizures
- focal neurological deficits
- headaches
- cerebral dysfunction: confusion, abnormal behaviour, memory disturbance, depressed concious level)
43
how could you perhaps differentiate between viral encephalitis and bacterial meningitis?
- onset of viral encephalitis is generally slower than for bacterial meningitis and cerebral dysfunction is a more prominent feature.
44
aetiology of encephalitis
- mainly viral with the most common pathogen being herpes simplex virus type 1 (HSV-1).
- other viral causes > varicella-zoster virus, epstein-barr virus, cytomegalovirus.
- meningitis > meningoencephalitis.
- autoimmune encephalitis.
45
what are features of auto-immune encephalitis caused by anti-VGKC (voltage gated potassium channel) antibodies?
- frequenct seizures
- amnesia (not able to retain new memories)
- altered mental state
46
anti-NMDA receptor antibodies are a feature of which autoimmune condition?
autoimmune encephalitis
47
what are the investigations of meningitis?
- blood cultures (bacteraemia)
- lumbar puncture (CSF culture/microscopy)
- no need for imaging if no contraindications to lumbar puncture (CT head if contraindicated).
48
what are the investigations of encephalitis?
- blood cultures and viral PCR
- imaging (CT scan +/- MRI)
- lumbar puncture (CSF analysis with viral PCR)
- EEG
49
what would CSF findings show in bacterial meningitis?
| Opening pressure, cell count (and type of WBC raised), glucose, protein
- opening pressure > increased.
- cell count > high, mainly neutrophils.
- glucose > reduced.
- protein > high.
50
what would CSF findings show in viral meningitis and encephalitis?
| opening pressure, cell count (and type of WBC), glucose, protein
- opening pressure > normal/increased.
- cell count > high, mainly lymphocytes.
- glucose > normal (60% of blood glucose).
- protein > slightly increased.
51
aetiology of Arbovirus encephalitides
- transmitted to man by vector (mosquito or tick) from non human host e.g.: West Nile virus.
52
describe a brain abscess
localised area of pus within the brain
53
what is a subdural empyema?
thin layer of pus between the dura and arachnoid membranes over the surface of the brain
54
what are the clinical features of brain abscess and empyema?
- fever
- headaches
- focal symptoms/signs: seizures, dysphasia, hemiparesis etc.
- signs of raised intracranial pressure: papilloedema, depressed conscious level.
- meningism may be present, particulary with empyema.
- features of underlying source e.g. dental, sinus or ear infection.
55
what are some causes of brain abscess and empyema?
- penetrating head injury
- spread from adjacent infection: dental, sinusitis, otitis media
- blood-borne infection e.g. bacterial endocarditis
- neurosurgical procedure
56
how do we diagnose brain abscess and empyema?
- CT or MRI.
- investigate source.
- blood cultures.
- biopsy (drainage of pus).
57
what are the most common organisms responsible for a brain abscess?
- streptococci in 70% of cases, especially the penicillin-sensitive kind: strep anginosus, strep intermedius, strep constellatus.
- anaerobes in 40-100% of cases: bacteroides, prevotella.
58
what is the management for a brain abscess?
- surgical drainage if possible
- penicillin or ceftriaxone to cover streptococcus (high dosage).
- metronidazole for anaerobes (high dosage).
- culture and sensitivity tests on aspirate provide useful guide
59
what are some HIV indicator illnesses affecting the brain?
- cerebral toxoplasmosis
- aseptic meningitis/encephalitis
- primary cerebral lymphoma
- cerebral abscess
60
del
del
61
which spirochaetes can infect the CNS?
- lyme disease (Borrelia burgdorferi)
- syphilis (trepomena pallidum)
- leptospirosis (leptospira interrogans)
62
describe stage 1 of lyme disease
| early localised infection (1-30 days)
- early localised infection (1-30 days)
- characteristic expanding rash at the site of the tick bite: erythema chronicum migrans (circular, target-shaped lesion)
- 50% flu like symptoms (days-1week): fatigue, myalgia, arthralgia, headache, fever, chills, neck stiffness)
63
describe stage 2 of lyme disease
| early disseminated disease, lasting from days to months
- early disseminated disease, lasting from days to months
- continued flu-like symptoms
- neuroborreliosis: facial nerve and other cranial nerve palsies, aseptic meningitis, encephalitis, peripheral mononeuritis etc.
- cardiovascular involvement: myocarditis, heart block and other arrhythmias, pericarditis
- early painful arthritis
64
describe stage 3 of lyme disease
| late disseminated disease, lasting from months to years
- late disseminated disease, lasting from months to years.
- arthritis
- late neurological disorders: polyneuropathy, chronic encephalomyelitis, dementia, psychosis
- acrdermatitis chronica atrophicans: blue-red discolouration and swelling at extensor surfaces
65
investigations for lyme disease
- complex range of serological tests
- CSF lymphocytosis
- MRI brain/spine (if CNS involvement)
- nerve conduction studies/EMG (if PNS involvement)
66
what is the treatment for Lyme disease?
- prolonged antibiotic treatment: IV ceftriaxone, oral doxycycline.
67
how is neurosyphilis treated?
high-dose penicillin
68
What is a prion disease? Give an example.
- Prion diseases are transmissible, untreatable, and fatal brain diseases of mammals. Their cause is highly unusual: The host's normal prion protein can, for unknown reasons, malfunction and assemble into structured aggregates called prions that cause infectious brain disease.
- Creutzfelt-Jakob disease (CJD)
69
signs and symptoms of Creutzfelt-Jakob disease (CJD)
- rapidly progressive dementia
- neurological symptoms including ataxia, weakness and visual disturbances
- psychiatric impairment, often preceding the neurological symptoms
- myoclonus, particulary triggered by startle
70
what is the prognosis of sporadic CJD?
- rapid progression
- death often within 6 months
71
what is the definition of Brown-Sequard syndrome?
characterised by anatomical disruption of nerve fibre tracts in one half of the spinal cord
72
clinical features of Brown-Sequard syndrome?
Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury:
- Ipsilateral hemiplegia
- Ipsilateral loss of proprioception and vibration
- Contralateral loss of pain and temperature sensation
73
myelopathy investigations
- localise: imaging- MRI best
- investigate cause: bloods, CSF
74
which artery is most commonly affected in a spinal cord stroke?
usually anterior spinal artery
75
what can cause a vitamin B12 deficiency?
- diet (vegans)
- pernicious anaemia
- total gastrectomy
- Crohn's disease
- tape worms
76
symptoms and signs of muscle disease
- weakness of skeletal muscle > respiratory and swallowing muscles important.
- cardiac symptoms (cardiomyopathy, arrhythmias).
- cramps/muscle pain, stiffness.
- myoglobinuria (muscle breakdown product in urine).
- babies: floppy, poor suckling/feeding/failure to thrive.
77
muscle disease investigations
- history and examination
- bloods especially creatine kinase (CK)
- electromyography (EMG)
- muscle biopsy: structure, biochemistry, inflammation
- genetic testing
78
what are some congenital/genetic causes of muscle disease?
- contractile: congenital myopathies
- structural: muscular dystrophies
- coupling: channelopathies
- energy: metabolic myopathies
79
what are some acquired causes of muscle disease?
- electrolyte disturbance (especially K+).
- endocrine: thyroid, adrenal, vitamin D.
- autoimmune inflammatory muscle disease.
- iatrogenic: medication (steroids/statins).
80
myasthenia gravis definition
- an autoimmune disease marked by the production of antibodies that target the nicotinic acetylcholine receptors on muscle fibres.
- reduces the ability of acetylcholine to trigger muscle contraction, resulting in muscle weakness.
81
signs and symptoms of myasthenia gravis
- limb muscle weakness
- extra-ocular muscle involvement leading to drooping eyelids (bilateral ptosis), diplopia (double vision)
- facial muscle involvement > difficulty smiling or chewing
- bulbar muscle involvement > change in speech or difficulty swallowing
- fatigable muscle weakness, bilateral ptsosis, a myasthenic snarl, head droop, and bulbar features on examination.
82
key investigations in the diagnosis of myasthenia gravis
- blood tests: testing for serum ACh receptor antibody and muscle-specific tyrosine kinase antibodies (anti-MUSK).
- CT chest to identify thymic hyperplasia or thymoma.
- nerve conduction studies/EMG: repetitive nerve stimulation testing
83
treatment of myasthenia gravis
- immunosuppressive therapy such as steroids
- anticholinesterase inhibitors such as pyridostigmine or neostigmine
- acute cases: IV immunoglovulin or plasmapheresis in severe, steroid-refractory cases
- thymectomy
84
what are causes of generalised peripheral neuropathy?
- hereditary
- metabolic: diabetes, alcohol, renal failure, vitamin deficiency
- toxic: drugs
- infectious: lyme disease, HIV, leprosy
- malignancy: paraneoplastic
- inflammatory (autoimmune), usually demyelinating: acute = Guillain Barre syndrome (post-infectious), chronic = chronic inflammatory demyelinating neuropathy.
85
symptoms and signs of peripheral nerve disease
- loss of sensation, abnormal sensation, pain.
- muscle thinning, weakness.
- skin changes, blood pressure, bowel and bladder changes.
86
peripheral nerve disease investigations
- blood tests
- nerve conduction studies/EMG
- lumbar puncture (CSF analysis)
- nerve biopsy
- genetic analysis
87
motor neuron disease definition
- a group of progressive neurological disorders that destroy motor neurons, the cells that control voluntary muscle activity such as speaking, walking, breathing and swallowing.
88
signs and symptoms of motor neurone disease
motor neurone disease typically manifests as a combination of upper and lower motor neurone signs
upper motor neuron signs include:
- spasticity
- hyperreflexia
- upgoing plantars (although they are often downgoing in MND)
lower motor neuron signs include:
- fasciculations
- muscle atrophy
89
motor neurone disease diagnosis
- unique combination UMN and LMN signs, no sensory involvement.
- electromyography
- genetic testing
90
what vertebrae is this? and what are its identifying features?
- C1 (atlas)
- ring-shaped
- has no body or spinous process but has large transverse processes with foramen transversium accommodating a vertebral artery on either side.
91
what vertebrae is this? what are its identifying features?
- C2 (axis)
- has body and a distinct 15mm (range 9-21mm) high odontoid process (dens).
92
what vertebrae is this? what are its distinguishing features?
- C7 vertebrae
- long, non-bifid spinous process
- transverse foramen and triangular vertebral canal
93
what are some distinguishing features of thoracic vertebrae?
- heart-shaped body
- small, circular spinal canal
- presence of costal facets
94
what are distinguishing features of lumbar vertebrae?
- massive kidney-shaped bodies
- no costal facets
95
how many spinal nerves are there?
31 pairs
96
how are the 31 pairs of spinal nerves divided into vertebral levels?
- 8 cervical
- 12 thoracic
- 5 lumbar
- 5 sacral
- 1 coccygeal
97
sensory info about fine touch, joint position, vibration and proprioception is transmitted via which tract?
dorsal column
98
sensory info about pain and temperature is transmitted via which tract?
lateral spino-thalamic tract
99
what brain defect occurs due to failure of the anterior neuropore to close during development?
anencephaly
100
what birth defect occurs due to failure of the posterior neuropore to close during development?
spina bifida
101
what substances obtained from amniocentesis can identify open neural tube defects in high-risk mothers?
alpha-fetoprotein (AFP) and acetylcholinesterase
102
describe spina bifida occulta
- incomplete fusion of the vertebrae, but with no herniation of the spinal cord.
- may be visible only as a small tuft of hair overlying site.
103
describe meningocele spina bifida
- incomplete fusion of the vertebrae, with herniation of a meningeal sac containing CSF.
- visible prominence at the site, but usually covered by skin.
104
describe myelomeningocele spina bifida
- incomplete fusion of the vertebrae with herniation of a meningeal sac containing CSF and spinal cord.
- usually accompanied by other defects such as hydrocephaly or Chiari malformation.
- visible prominence at site, with exposed meninges.
105
clinical manifestations of spina bifida
neurological:
- motor deficits
- sensory deficits
- neurogenic bladder or bowel
- hydrocephalus
- seizures
musculoskeletal:
- increased risk of hip subluxation
- scoliosis
- contractures
106
treatment for spina bifida
- primary neurosurgical repair
- orthopaedic surgery
107
what are the most commonly isolated organisms in pyogenic vertebral osteomyelitis and discitis?
- gram-positive organisms such as Staph.aureus and Streptococcus species.
108
symptoms and signs of pyogenic vertebral osteomyelitis and discitis
- axial pain
- fever
- neurological changes: radicular numbness, muscle weakness
109
pyogenic vertebral osteomyelitis and discitis treatment
- administration of broad-spectrum IV antibiotics for at least 6-8 weeks until culture-specific regimens may be initiated.
- immobilisation may be beneficial for reducing pain and stabilising spine.
- if needed, surgery: debridement, decompression of neural structures and stabilisation of the spine.
110
how are spinal cord tumours classified?
111
what is the gold-standard imaging investigation of spinal cord tumours?
MRI
112
best imaging modality for spinal hematomas?
MRI
113
treatment of spinal hematomas
- correction of coagulopathy if present, emergency surgical decompression if their is a neurological deficity (usually involves laminectomy).
114
cauda equina syndrome definition
a surgical emergency that results from compressive, ischaemic, and/or inflammatory neuropathy of multiple lumbar and sacral nerve roots in the lumbar spinal canal.
115
how does cauda equina syndrome present clinically?
- leg pain, weakness, anaesthesia
- saddle anaesthesia
- bladder, bowel and sexual dysfunction
- decreased anal tone
- absence of ankle reflex
116
what is the gold-standard imaging modality for cauda equina syndrome?
MRI
117
what is the treatment for cauda equina syndrome
surgical decompression within 24 hours seems to have best outcomes
118
what is the most commonly affected spinal segment in spinal cord injury?
cervical
119
what is the pathology of a primary spinal cord injury?
trauma results in the immediate death of local cells:
1. direct damage to cell bodies and/or neuronal processes (die and not replaced)
2. damage to spinal axons (undergoes Wallerian degeneration)
120
pathology of secondary spinal cord injury
1) inflammation
2) vascular events: diminished blood flow > ischemia > inflammation and secondary tissue damage
3) chronic pahse of injury which includes: demyelination and scar formation
121
spinal shock definition
- transient loss of all neurologic function below level of the spinal cord injury > flaccid paralysis and areflexia (loss of bulbocavernosus reflex).
- hypotension
- duration: 72 hours, but typically persists 1-2 weeks, occasionally several months
122
what can cause spinal shock?
- interrupyion of sympathetics: implies spinal cord injury above T1
- loss of vascular tone (vasoconstrictors) below level of injury leaves parasympathetics relatively unopposed causing bradycardia
- relative hypovolemia: skeletal mucle paralysis below level of injury results in venous pooling
- true hypovolemia: due to blood loss from associated wounds
123
how is resolution of spinal shock firstly recognised?
return of bulbocavernosus reflex
124
what are types of incomplete spinal cord injury called?
- central cord syndrome
- Brown-Sequard syndrome
- anterior cord syndrome
- posterior cord syndrome
125
what type of movement is associated with central cord syndrome?
usually results from hyperextension injury in older patient with pre-existing stenosis
126
central cord syndrome clinical presentation
- motor: weakness in upper limb more than lower limb
- sensory: loss below the level of injury
- sphincter: urine retention
127
what usually causes anterior cord syndrome?
- occlusion of the anterior spinal artery
- anterior cord compression e.g. by dislocated bone fragment or by traumatic herniated disc
128
clinical presentation of anterior cord syndrome
- paraplegia, or quadraplegia (if higher than C7)
- dissociated sensory loss below lesion: loss of pain and temperature sensation (spinothalamic tract lesion) with preservation of posterior column function (touch, proprioception, vibration etc.).
129
how does Brown Sequard sydrome manifest?
- ipsilateral loss of joint position sense, vibration sense and discrimination (posterior columns).
- ipsilateral spastic paresis below the level of lesion (pyramidal tract).
- contralateral loss of pain and temperature one level below the lesion (lateral spinothalamic tract).
130
multiple sclerosis definition
Multiple sclerosis is a chronic autoimmune disease, primarily involving the central nervous system, which is marked by the degeneration of the insulating covers of nerve cells in the brain and spinal cord, leading to demyelination and eventual axonal loss.
131
signs and symptoms of MS
- sensory disease, marked by patchy paraesthesia
- optic neuritis, characterised by loss of central vision and painful eye movements
- internuclear opthalmoplegia, a lesion in the medial longitudinal fasciculus of the brainstem
- subacute cerebellar ataxia
- spastic paraperesis
- bladder and bowel involvement
132
pathology of MS
Pathologically, CD4-mediated destruction of oligodendroglial cells and a humoral response to myelin binding protein are key features of the disease.
133
classification of MS
- relapsing-remitting (85% at outset)
- secondary progressive
- primary progessive (10-15%)
134
discuss the diagnosis of MS
based on at least two of:
- clinical history/exam
- imaging findings: typically these are periventricular white matter lesions seen on MRI
- oligoclonal badnds in CSF
135
which criteria are used for an MRI based diagnosis of MS?
Posers criteria (clinical)
Macdonald criteria (MRI)
136
acute management of MS
- exclude infection
- oral prednisolone (intravenous)
- rehab
- symptomatic treatment
137
what are symptomatic therapies for MS
- Physiotherapy
- Baclofen and Botox for spasticity
- Modafinil and exercise therapy for fatigue
- Anticholinergics for bladder dysfunction
- SSRIs for depression
- Sildenafil for erectile dysfunction
- Clonazepam for tremor
138
what disease-modifying therapies are used to treat MS?
- First-line injectables such as beta-interferon and glatiramer acetate
- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
- Biologics such as natalizumab and alemtuzumab.
139
what are the three categories of syncope?
reflex (neuro-cardiogenic):
- taking blood/medical situations
- cough, micturation
orthostatic:
- dehydration, medication related (anti-hypertensive)
- endocrine, autonomic nervous system
cardiogenic:
- arrhythmia, aortic stenosis
140
epilepsy definition
Epilepsy is a neurological disorder characterized by an enduring predisposition to generate epileptic seizures due to abnormal excessive or synchronous neuronal activity in the brain.
141
factors increasing seizure risk
- missed medications (most common)
- sleep disturbance, fatigue
- hormonal changes
- drug/alcohol use, drug interactions
- stress/anxiety
- photosensitivity in a small group of patients - other rarer reflex epilepsies (visual patterns, music)
142
how do we classify generalised seizures?
- absence seizures
- generalised tonic-clonic seizures
- myoclonic seizures
- juvenile myoclonic epilepsy
- atonic seizures
143
how do we classify focal seizures?
- focal seizure with retained awareness
- focal seizure with loss of awareness
- focal to bilateral convulsive seizures (secondary generalised)
- or by location of onset (temporal lobe, frontal etc.)
144
what are features of primary generalised epilepsies?
- no warning before seizure
- <25 years old
- may have a histroy of absences and myoclonic jerks as well as GTCS e.g. in juvenile myoclonic epilepsy
- generalised abnormality on EEG
- may have a family history
145
what are features of focal/partial epilepsies?
- may get an 'aura'
- any age- cause can be any focal brain abnormality
- simple partial and complex partial seizures can become secondary generalised
- focal abnormality on EEG
- MRI may show cause
146
epilepsy investigations
- detailed clinical history and neurological examination
- electroencephalogram (EEG) for primary generalised epilepsies including hyperventilation and photic stimulation: sometimes sleep deprivation
- MRI for patients under 50 with possible focal onset seizures
- CT usually adequate to exclude serious causes >50
- video-telemetry if uncertain about diagnosis
147
first and second line drugs for status epilepticus?
- first line: lorazepam, midazolam (diazepam)
- second line: valproate, levetiracetam or phenytoin
148
what drugs are used for primary generalised epilepsies?
first line:
- sodium valproate
- levetiracetam
- lamotrigine
second line:
- topiramate
- zonisamide
- clobazam
- (carbamazepine)
149
what drugs are used for focal and focal to bilateral convulsive seizures?
lamotrigine
carbamazepine
levetiracetam
150
side effects os sodium valproate
- tremor
- weight gain
- ataxia
- nausea
- drowsiness (encephalopathy)
- hepatitis
- bone marrow suppression
- drug-induced parkinsonism
- avoid in women of childbearing age
151
side effects of carbamazepine
ataxia
drowsiness
nystagmus
blurred vision
low serum sodium levels
skin rash
152
side effects of lamotrigine
skin rash
difficulty sleeping
153
side effects of levetiracetam
irratibility
depression
154
describe status epilepticus
- prolonged or recurrent tonic-clonic seizures persisting for more than 30 minutes with no recovery period between seizures.
- usually occurs in patients with no previous history of epilepsy (stroke, tumour, alcohol).
- mortality 5-10%
155
what are possible functions of CSF?
- shock absorber for CNS
- immunological function analogous to lymphatic system
156
what is the production rate and turnover of CSF in adults?
- produced at a rate of about 0.3 ml/min > approx 450ml/24 hours.
- CSF is turned over 3 times every day.
157
describe a lumbar puncture
used to harvest sample of CSF
158
what is hydrocephalus?
an abnormal accumulation of cerebrospinal fluid within the ventricles of the brain
159
how can hydrocephalus be categorised?
Hydrocephalus can be categorised into non-communicating (obstructive) and communicating types, each with its own causes.
- non-communicating > an obstruction in the ventricular system disrupts the flow of CSF.
- communicating > CSF is not adequately reabsorbed due to damage to the arachnoid villi.
160
what conditions can cause non-communicating (obstructive) hydrocephalus?
- Congenital malformations such as aqueduct stenosis or a Chiari malformation and/or myelomeningocele
- A tumour or vascular malformation in the posterior fossa
- An intraventricular haemorrhage (premature infants are particularly at risk)
161
which conditions can cause communicating hydrocephalus?
- Meningitis
- Subarachnoid haemorrhage
162
signs and symptoms of hydrocephalus in infants
- An enlarged head circumference, noticeable upon inspection or when tracking their growth
- Bulging of the anterior fontanelle
- Distention of scalp vein
- 'Sunsetting' of the eyes, a late sign where upward gaze is limited due to raised intracranial pressure
- irritability, poor head control
163
signs and symptoms of hydrocephalus in older children (with rigid cranial vault) and adults
symptoms are those of increased ICP:
- papilledema
- H/A (headache)
- N/V (nausea and vomiting)
- gait changes
- upgaze and/por abducens palsy
- slowly enlarging ventricles may initially be asymptomatic
164
hydrocephalus investigations
- A cranial ultrasound through the anterior fontanelle, typically conducted during the first few months of life when the fontanelle is still open
- MRI or CT of the brain, offering detailed images to assess ventricular size and identify potential underlying causes such as tumours or haemorrhages
165
hydrocephalus treatment
- lumbar puncture
- lumbar drain
- external ventricular drain
- endoscopic third ventriculostomy
- ventriculo-peritoneal shunt
166
what is the most likely causative organism in neonatal meningitis?
group B streptococcus
167
meningioencephalitis is a complication most commonly associated with which condition?
mumps
