Neurology Flashcards
(170 cards)
1
Q
Describe the tract of the olfactory nerve.
A
- olfactory cells of nasal mucosa
- olfactory bulbs
- pyriform cortex via cribriform plate
2
Q
Describe the tract of the optic nerve.
A
- retinal ganglion cells
- optic chiasm
- optic tract
- lateral geniculate body
- optic radiation
- primary visual cortex in occipital cortex
3
Q
What should you examine when testing the optic nerve?
A
- optic discs with ophthalmoscope
- pupillary responses
- visual acuity (using Snellen chart)
- visual fields and blind spot
4
Q
Discuss the papillary light reflex.
A
- retinal ganglion cells
- optic nerve
- pretectal area
- synapse with Edinger-Westphal nucleus
- parasympathetic signals via oculomotor nerve which synapse with ciliary ganglion
- post-synaptic nerves innervate iris sphincter muscle
5
Q
An optic tract lesion of which area would cause bitemporal hemianopia?
A
optic chiasm
6
Q
A lesion of the optic tract would lead to which visual field defect?
A
contralateral homonymous hemianopia
7
Q
Which visual tract defect arises from a right sided Meyer’s loop lesion?
A
left homonymous superior quadrantanopia
8
Q
Right homonymous inferior quadrantanopia is caused by a lesion where?
A
left optic radiations before they are joined by fibres from Meyer’s loop
9
Q
List the structures that the oculomotor nerve innervates.
A
Motor: inferior oblique, superior, medial and inferior recti muscles AND levator palpebrae superioris
Para: ciliary muscle, pupillary constrictor muscles
10
Q
Which nerve supplies the superior oblique muscle and what movement does it cause?
A
- trochlear nerve
- depresses adducted eye and intorts abducted eye
11
Q
What is internuclear ophthalmoplegia?
A
failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye
12
Q
What causes internuclear ophthalmoplegia? Which disease is it commonly seen in?
A
results from lesion of medial longitudinal fasiculus
MS
13
Q
What results from ipsilateral disruption of cervical sympathetic chain?
A
Horner’s syndrome
14
Q
List the features seen in Horner’s syndrome.
A
- miosis
- ptosis
- anhidrosis
- apparent enophthalmos
15
Q
Name some causes of cervical sympathetic chain disruption.
A
congenital, brainstem stroke, cluster headache, apical lung tumour, MS, carotid artery dissection
- cervical rib
- syringomyelia
16
Q
Describe the function of the trigeminal nerve.
A
- sensory: face (ophthalmic, mandibular, maxillary) and anterior 2/3 tongue
- motor: masseter, temporalis, medial and lateral pterygoids
17
Q
Which sensory component of the trigeminal nerve does herpes zoster ophthalmicus affect? How is it treated?
A
V1
oral aciclovir
18
Q
Describe the function of the facial nerve.
A
motor: muscles of facial expression
sensory: taste (anterior 2/3 tongue)
para: salivary and lacrimal glands
19
Q
What clinical differences are seen between upper and lower facial motor neurone lesion?
A
upper: weakness of inferior facial muscles
lower: weakness of superior and inferior facial muscles
20
Q
Describe the corneal reflex. (3 points)
A
- lightly touch cornea with cotton wool
- afferent = V
- efferent = VII
- test of pontine function
21
Q
What is the function of CNVIII? What structures does it innervate?
A
vestibulocochlear nerve
balance: nerve endings within semi-circular canals to cerebellum and spinal cord
hearing: cochlear to auditory cortex in temporal lobes
22
Q
Discuss the function of the glossopharyngeal nerve and the structures it innervates.
A
- sensory: taste (posterior 1/3 tongue), proprioception for swallowing (pharyngeal wall), blood pressure receptors (carotid sinuses)
- motor: swallow and gag reflexes (pharyngeal muscles), lacrimation (lacrimal glands)
- para: salivation (parotid glands)
23
Q
What is seen in glossopharyngeal palsy?
A
deviation of uvula away from the side of lesion
24
Q
Discuss the function of the vagus nerve and the structures it innervates.
A
- sensory: chemoreceptors (blood oxygen conc, carotid bodies), pain receptors (resp and GI tract), sensation (external ear, larynx, pharynx)
- motor: HR and stroke volume (pacemaker and ventricles), peristalsis (GI tract smooth muscles), air flow (bronchial smooth muscles), speech and swallowing (larynx and pharynx)
- para: smooth muscles and glands of same areas as motor, as well as thoracic and abdo areas
25
What is the function of the spinal accessory nerve?
head rotation and shoulder shrugging - sternocleidomastoid and trapezius muscles
26
Which nerve is responsible for the motor component of the tongue?
hypoglossal
27
What would be seen in a left-sided hypoglossal palsy?
tongue deviation to left
28
Discuss the nucleus location of each of the cranial nerves.
forebrain: I, II
midbrain: III, IV
pons: V, VI, VII, VIII
medulla: IX, X, XI, XII
29
Which cranial nerves exit the skull via the superior orbital fissure?
III, IV, V1, VI
30
Discuss where the three components of the trigeminal nerve exit the skull.
V1: superior orbital fissure
V2: foramen rotundum
V3: foramen ovale
31
CN VII and VIII exit the skull through what?
internal acoustic meatus
32
The jugular foramen allows the passage of which cranial nerves and vessels?
IX, X and XI
internal jugular vein
sigmoid and internal petrosal sinus
33
CN XII exits the skull via which canal?
hypoglossal canal
34
Discuss radial nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.
- entrapment at spiral groove 'saturday night palsy'
- wrist and finger drop, usually painless
- sensory: lateral aspect of back of hand
motor: wrist and finger extension, elbow flexion in mid-pronation (brachioradialis)
35
Discuss ulnar nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.
- entrapment at medial epicondyle (ulnar groove)
- history of trauma to elbow, weak grip, usually painless
- sensory: medial aspect of hand
motor: wrist flexion, index and pinkie abduction, thumb adduction
36
Discuss median nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.
- entrapment within carpal tunnel at wrist
- history of intermittent nocturnal pain, numbness and tingling (often relieved by shaking hand), positive Tinel's sign/Phalen's test, weak grip
- sensory - lateral palm of hand
- motor: LOAF
37
Discuss femoral nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.
- haemorrhage/trauma
- weakness of quadriceps and hip flexion, numbness in medial skin
- sensory - lateral leg
- motor - knee extension, hip flexion and adduction
38
Discuss common peroneal nerve palsy including: causes, presenting symptoms, sensory change and motor weakness.
- entrapment of fibular head
- trauma, surgery or external compression, acute onset foot drop, usually painless
- sensory: lateral leg
- motor: ankle dorsiflexion, great toe extension
39
What is mononeuritis multiplex? List some common causes.
simultaneous or sequential development of nerve palsy of 2 or more nerves
causes: diabetes, vasculitic, RA, lupus, Sjogren's syndrome, hep C, HIV, sarcoidosis, lymphoma
40
Distinguish between a primary and secondary headache including examples of each.
```
primary = headache and its ass. features is the disorder (no underlying cause) e.g. migraine, tension, cluster
secondary = secondary to underlying causes e.g. subarachnoid haemorrhage, space-occupying lesion, meningitis, temporal arteritis
```
41
List some 'red flag' features which suggest secondary headache.
Systemic symptoms (fever, weight loss)
Neurological signs or symptoms
Older age of onset
Onset is acute ( <5 mins)
Previous headache history is different or absent
Triggered headache (valsalva, exertion or posture)
42
Which signs suggest a secondary headache on examination?
systemic: reduced conscious level, BP, pyrexia, meningism, skin rash, temporal artery tenderness
cranial nerve: pupillary responses, visual fields, eye movements, fundoscopy
43
Name 4 upper motor neurone signs to look for in headache clinical exam.
- pronator drift
- increased tone
- brisk reflexes
- extensor plantar response
44
Name 4 cerebellar signs that may be seen in headache examination.
- nystagmus
- past-pointing
- dysdiadochokinesis
- broad-based ataxic gait
45
Give a description of the pathophysiology of migraine.
- primary dysfunction in brainstem sensory nuclei (V, VII - X)
- pain results from pain sensitive cranial blood vessels and their innervating trigeminal fibres
- aura: cortical spreading depression
46
List the stages of migraine and give a description of each.
- prodrome - up to 48 hrs before headache, mood disturbance, restlessness, hyperosmia, photophobia, diarrhoea
- aura - recurrent reversible focal neurological symptoms, develops over 5-20 mins and lasts <60mins, visual aura (scotoma, flashing lights, fortification spectrum), sensory aura often starts in hand and migrates up arm
- headache - throbbing or pulsatile, moderate-severe, gradual onset, 4-72 hours, unilateral in 60%, can radiate, aggravated by routine physical activity
- associated symptoms - N&V, photophobia, phonophobia, osmophobia, mood disturbance, diarrhoea
- postdrome
47
Give examples of visual aura seen in headache.
zigzag fortification spectrum, visual field loss, negative scotoma, positive scotoma
48
What are two complications of migraine?
1. Medication overuse headache: headache 15+ days per month associated with frequent use of acute relief meds
2. Chronic migraine: headache on 15+ days per month
49
Discuss the management of migraine.
- lifestyle: avoid triggers, reduce caffeine/alcohol, encourage regular meals and sleep patterns
- acute management: simple analgesia, triptans, antiemetic
- prophylaxis: beta-blockers, tricyclic antidepressants, anti-epilepsy
50
Define a thunderclap headache.
abrupt-onset of severe headache which reaches maximal intensity <5mins (and lasts >1hr)
should be considered as subarachnoid haemorrhage until proven otherwise
51
What are the causes of thunderclap headache?
- subarachnoid haemorrhage
- intracerebral haemorrhage
- arterial dissection
- cerebral venous sinus thrombosis
- bacterial meningitis
- primary headaches
52
How do you investigate a thunderclap headache?
- bloods
- 12 lead ECG
- urgent CT brain
- lumbar puncture (xanthochromia - subarachnoid haemorrhage)
53
What is a normal intracranial pressure?
7-15 mmHg
54
What are some causes of increased ICP?
- mass effect: tumour, infarction with oedema, haematoma, abscess
- increased venous pressure
- obstruction to CSF flow/absorption: hydrocephalus, meningitis
- idiopathic
55
What are some key history findings in a raised pressure headache?
- worse on lying flat, improved on sitting
- worse in morning
- persistent N&V
- worse on valsalva
- worse with physical exertion
- transient visual obscurations with change in posture
56
List some examination findings in raised pressure headaches.
- optic disc swelling - papilloedema
- impaired visual acuity
- restricted visual fields
- CN III palsy
- CN VI palsy
- focal neurological signs
57
What are the two major causes of low pressure headache?
- post-lumbar puncture - most resolve spontaneously
| - spontaneous intracranial hypotension - spontaneous dural tear, following valsalva
58
Does lying down relieve a high or low pressure headache?
low
59
Discuss the clinical presentation of neuropathy including motor, sensory and autonomic.
motor: weakness/muscle atrophy
sensory: large - sensory ataxia/loss of vibration sense/numbness/tingling, small - impaired pin prick/temperature/painful burning/numbness/tingling
autonomic: postural hypotension, erectile dysfunction, GI disturbance, abnormal sweating
60
Define length-dependent axonal neuropathy.
- diffuse involvement of peripheral nerves
- age > 50 yrs
- starts in toes/feet
- symmetrical and slowly progressive
61
What are some causes of length-dependent axonal neuropathy?
- diabetes
- alcohol
- nutrition deficiency (B12 and folate)
- others: immune e.g. RA, lupus, renal failure, hypothyroidism, drugs, infections, myeloma
62
What is Guillain-Barre syndrome?
- acute inflammatory autoimmune demyelinating neuropathy
- progressive ascending weakness over days
- flaccid, quadraparesis with areflexia +/- respiratory/bulbar/autonomic involvement
63
Describe the aetiology of GB.
post-infectious autoimmune e.g. camplyobacter, CMV, EBV
64
How is GB treated?
IV Ig or apheresis
65
Define myasthenia gravis.
autoimmune disorder: antibodies to ACh receptor at post-synaptic NMJ - fatiguable weakness of ocular, bulbar, neck, resp and/or limb muscles
66
What is myasthenia gravis associated with?
other autoimmune disorders
| ? thymic hyperplasia and thymoma
67
What investigations should be carried out if myasthenia gravis is suspected?
- antibodies to AChR present
| - abnormal single fibre EMG and repetitive nerve stimulation
68
Discuss the management of myasthenia gravis.
- pyridostigmine (anti-ACh esterase)
| - immunosuppressive therapies (steroids and IV Ig)
69
Give a detailed definition of stroke.
central nervous system infarction (which includes brain, spinal cord and retinal cells attributable to ischaemia), based on objective evidence of focal ischaemic injury in a defined vascular distribution or clinical evidence of the former with other aetiologies excluded.
70
What are the signs and symptoms of stroke?
- acute onset
- right weakness: leg/face and arm/hemiparesis (sensory and motor cortex)
- dysphasia (Broca's and Wernicke's area)
- visual disturbance: right homonymous heminopia (optic tract runs in MCA region)
- acute light-headedness
71
List four classes of stroke according to Oxfordshire Community Stroke Project.
1. Total anterior circulation syndrome: proximal MCA or ICA occlusion - hemiparesis, hemianopia, higher cortical dysfunction
2. Partial anterior circulation syndrome: branch MCA occlusion - isolated higher cortical dysfunction or 2 of: hemiparesis, hemianopia, higher cortical dysfunction
3. Posterior circulation syndrome: perforating arteries, PCA, cerebellar occlusion - isolated hemianopia or brainstem syndrome
4. Lacunar syndrome: perforating artery/small vessel disease - pure motor or pure sensory or sensorimotor stroke or ataxic hemiparesis or clumsy hand-dysarthritis
72
Define intracerebral haemorrhage.
a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma
73
Define stroke caused by intracerebral haemorrhage.
rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma
74
List common causes of an intracranial bleed.
```
trauma
small vessel disease
amyloid angiopathy
blood vessel abnormalities
blood clotting deficiencies
tumours
drugs: cocaine, amphetamine
```
75
Describe the differences in treatment approach in ischaemic stroke vs haemorrhagic stroke.
ischaemic: IV thrombolysis, thromboectomy aspirin, stroke unit, hemicranectomy
haemorrhagic: BP control, stroke unit, neurosurgical evaluation
76
3% of strokes are caused by aneurysmal SAH. How do aneurysms form and rupture?
- increased haemodynamic stress
- activation of endothelial cells
- recruitment of inflammatory cells
- outward vascular remodelling
- adapted and stabilised aneurysm
- sustained inflammation and remodelling leads to rupture
77
List predisposing factors that may lead to aneurysmal SAH.
- smoking
- female sex
- hypertension
- positive family history
- ADPCK, coarctation of aorta
78
What are the clinical history and examination findings in ASAH?
history: sudden onset headache, LOC, seizures, visual, speech and limb disturbances, sentinel headache
exam: photophobia, meningism, subhyaloid, haemorrhages, vitreous haemorrhages, speech and limb distrubances, pulmonary oedema
79
What is the use of CT in the investigation of ASAH?
- confirms diagnosis
- clues to aetiology
- identifies complications: infarction, haematoma, hydrocephalus
- prognostic: Fisher grade
80
Besides CT, what other investigations are useful in ASAH?
- LP: xanthochromia
- MRA
- DSA: stroke, diabetes
- hyponatraemia
- ECG changes
- elevated troponin levels
- ECHO
81
Describe the resuscitation process following ASAH.
- bed rest
- fluids - saline
- anti-embolic stockings
- nimodipine
- analgesia
- doppler studies
82
How can cerebral artery aneurysms be managed?
- surgical clipping
- endovascular coils, stents and glue
- conservative
83
What are the complications associated with aneurysms and how would you manage them?
- rehaemorrhage - immediate repair
- delayed ischaemia - fluid management, nimodipine, inotropes, angioplasty
- hydrocephalus - LP, shunt
- hyponatraemia - hypertonic saline, fludrocortisone
- ECG changes
- LRTI, PE, UTI
- seizures
- DVT
84
What is consciousness and what factors affect it?
it reflects level of arousal and presence of cognitive behaviour
factors: trauma, elevated ICP, fever, seizure, sepsis, medications etc.
85
Describe the scoring used in the Glasgow Coma Scale in adults.
```
EYE OPENING
4 spontaneous
3 to verbal command
2 to pain
1 none
VERBAL
5 oriented
4 confused
3 inappropriate
2 incomprehensible sounds
1 none
MOTOR
6 obeys command
5 localised pain
4 normal flexion
3 abnormal flexion
2 extension
1 none
```
86
How is GCS modified for young children?
verbal scale is not appropriate in non-verbal children
5 appropriate words, smiles, fixes/follows
4 consolable crying
3 persistently irritable
2 restless, agitated
1 none
87
How is GCS used to classify head injury?
14-15: minor
9-13: moderate
<8: severe
88
Discuss the WFNS grading system of SAH.
```
I: GCS 15 and -ve focal signs
II: GCS 13-14 and -ve focal signs
III: GCS 13-14 and +ve focal signs
IV: GCS 7-12 and +/-ve focal signs
V: GCS 3-6 and +/-ve focal signs
```
89
What is multiple sclerosis?
- idiopathic inflammatory demyelinating disease of CNS
- acute episodes of inflammation are associated with focal neurological deficits e.g. weak leg, visual loss and urinary incontinence
- deficits usually develop gradually, last for more than 24hrs and may gradually improve over days to week
- later in untreated disease patients becomes more disabled
90
List subtypes of MS.
- primary progressive MS
- secondary progressive MS
- benign MS
- relapsing remitting MS
- progressive relapsing MS
91
Name some syndromes that can develop into MS.
- optic neuritis
- clinically isolated syndromes
- transverse myelitis
- radiologically isolated syndromes
92
Discuss optic neuritis in relation to MS.
- painful visual loss that comes on over a few days caused by inflammation of optic nerve
- 30% develop MS by 5yrs
- 50% develop MS by 15yrs
- risk of MS depends on MRI scan and oligoclonal bands
93
Discuss transverse myelitis in relation to MS.
- inflammation of the spinal cord
- weakness
- sensory loss
- incontinence
94
What are clinically isolated syndromes relating to MS?
- single episode of neurological disability due to focal CNS inflammation
- may be first attack of MS
- can happen after infection and not be related to MS
95
What is the criteria for MS diagnosis?
MS is diagnosed when there is evidence of 2 or more episodes of demyelination disseminated in space and time
96
What causes MS?
genetic factors, sunlight/vit D exposure, viral trigger (EBV), smoking
97
When would you suspect MS?
- neurological symptoms that develop over a few days
- a history of transient neurological symptoms that have lasted for more than 24hrs and spontaneously resolved
- 'hidden relapses' e.g. optic neuritis, bell's palsy, labyrinthitis, sensory symptoms, bladder symptoms
98
List common symptoms of MS.
- optic neuritis
- nystagmus
- dysarthria
- dysphagia
- muscle weakness and spasm
- paraesthesia
- bowel and urinary incontinence
- diarrhoea or constipation
- urinary frequency or retention
99
How would you investigate suspected MS?
1. MRI brain and cervical spine with gadolinium contrast:
- demyelination in 2 regions can indicated dissemination in space
- enhancing and non-enhancing areas of demyelination can indicate dissemination in time
2. LP - oligoclonal bands, cell counts, glucose, protein
3. Bloods - exclude other conditions
4. Visual evoked potentials - subclinical optic neuritis
5. CXR - exclude sarcoidosis
100
What are oligoclonal bands and what is their relevance in MS?
- Ig bands seen in blood and spinal fluid after protein electrophoresis
- presence of bands in CSF but not blood suggests Ig production in CNS
- supports diagnosis of MS but can be seen in other conditions
101
Define relapse in relation to MS.
a relapse usually involves a new neurological deficit that lasts for more than 24hrs in the absence of pyrexia or infection
102
Define pseudo-relapse in relation to MS.
a pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old area of demyelination in the contect of pyrexia or infection
103
How is relapse in MS managed?
- 1g of IV methylprednisilone for 3 days or 500mg of oral methylprednisiline for 5 days
AND
- PPI for gastroprotection
- ideally prescribe at 9am to avoid sleep disruption
104
Discuss the medications available for MS.
dimethyl fumurate, alemtuzamab, natalizumab
105
What is the definition of dementia?
- progressive cognitive decline
- interfere with the ability to function at work or at usual activities
- represent a decline from previous levels of functioning and performing
- is not explained by delirium or major psychiatric disorder
106
Describe the cognitive history of a patient with dementia.
MEMORY - impaired ability to acquire and remember new information e.g. repetition, forgetfulness, getting lost
EXECUTIVE FUNCTION - impaired reasoning and handling of complex tasks, poor judgement e.g. poor decision making, poor risk assessment, poor financial management
VISUOSPATIAL - impaired visuospatial abilities e.g inability to recognise faces, can't dress or cook for self
LANGUAGE - impaired language functions e.g. difficulty thinking of words, speech hesitations
107
What is the purpose of the Addenbrokes cognitive assessment? And what does it examine?
- 100 questions to assess severity and pattern of impairment in dementia
- examines memory, attention/concentration, language, visuospatial, executive function
108
Which type of disorder is likely in deficit in ACEr of:
1. Episodic memory
2. Semantic memory
3. Attention/conc
4. Naming/fluency
5. Visuospatial
1. Alzheimer's
2. Semantic dementia - frontotemporal dementia
3. Delirium
4. Progressive non-fluent aphasia
5. PD plus syndrome or variants AD
109
How are seizure and epilepsy related?
seizure - episode of neuronal hyperactivity
| epilepsy - at least two unprovoked episodes of seizure
110
What are the features of focal (partial) epilepsy?
- history trauma/birth injury
- focal aura/sequelae (including gustatory/sensory/motor features) e.g. left arm increased tone = right sided motor area lesion
- post-attack confusion/drowsiness
- automatisms - plucking movements or fiddling, precedes seizures
- nocturnal events
- long lasting deja vu
111
What are the features of genetic generalised epilepsy?
- photosensitivity
- age of onset = 8-26
- alcohol or sleep deprivation
- myoclonus
- lack of aura
- seizures within 2hrs of awakening
- family history of IGE
- EEG abnormal
112
What are the DDx for epilepsy?
- syncope
- non-epileptic attack disorder
- migraine
- narcolepsy
- transient global amnesia
- panic attacks
113
Define status epilepticus.
>2 seizure without full recovery of neurological function between seizures
OR
continuous seizure activity >30 mins
MEDICAL EMERGENCY with recognised mortality
114
Name the three drugs normally used in the treatment of focal epilepsy.
lamotrigine
carbamazepine
levetiracetam
115
Name the three drugs normally used in the treatment of generalised epilepsy.
valproate
levetiracetam
lamotrigine
116
What should you do if you see someone in a seizure?
- keep them out of harm's way
- put them in recovery position
- if movements stop and no impairment of ABCs, does not need hospitalisation once recovers awareness
117
Discuss the pathology of Parkinson's disease.
- loss of dopaminergic neurones within substantia nigra
- surviving neurones contain Lewy bodies
- PD manifests clinically after loss of approx. 50% of dopaminergic neurones
118
What are some of the suggested mechanisms for LB formation?
- oxidative stress
- mitochondrial failure
- excitotoxicity
- protein aggregation
- interference with DNA transcription
- nitric oxide
- inflammation
- apoptosis
- trophin deficiency
- infection
119
Describe the pathological progression of PD.
Six stages:
1-2: medulla/pona and olfactory nucleus = presymptomatic or premotor e.g. loss of smell
3-4: midbrain - substantia nigra = parkinsonism
5-6: neocortex involvement = development of PD dementia
120
What are the main clinical parkinsonism features?
- bradykinesia - slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
- resting tremor - asymmetric
- rigidity
- postural instability
121
List some of the non-motor symptoms of PD.
- neuropsychiatric: dementia, depression, anxiety
- autonomic: constipation, nocturia, erectile dysfunction, sweating, postural hypotension
- sleep: REM sleep behaviour disorder, restless legs syndrome
- other: reduced olfactory function, fatigue, pain and sensory symptoms
122
What investigations would you undertake in suspected PD?
- bloods: TFTs, copper/caeruloplasmin
- structural imaging: CT/MRI brain normal in PD, abnormal in vascular parkinsonism
- functional imaging: imaging of presynaptic dopaminergic function using DAT SPECT is abnormal in degenerative parkinsonism
123
Discuss the treatment of PD.
- L-dopa
- dopamine agonists
- MAO-B inhibitors
- COMT inhibitors
- advanced stage = deep brain stimulation of subthalamic nucleus
124
Discuss the use of L-dopa in PD.
- taken up by dopaminergic neurones and decarboxylate to dopamine within presynaptic terminals
- prescribed alongside carbidopa which reduced side effects
125
What are the adverse effects and long term motor complications of L-dopa?
- peripheral: N&V, postural hypotension
- central: confusion, hallucinations
- fluctuations in motor response after 5 yrs
- dyskinesia
126
Ropinirole and pramipexole are examples of which type of PD drug? And how do they work?
dopamine agonists - act directly on post-synaptic striatal dopamine receptors (D2)
127
What are the side effects of dopamine agonists?
dopaminergic side effects and somnolence, impulse control disorders and nightmares
128
Which type of drug works by preventing dopamine breakdown by binding irreversibly to monoamine oxidase?
MAO-B inhibitors e.g. selegiline, rasagiline
129
Name two COMT inhibitors and describe their mechanism of action.
entacapone, tolcapone - inhibit catechol-o-methyltransferase results in longer L-dopa half life
130
Discuss the degenerative and secondary causes of parkinsonism.
- degenerative: dementia with Lewy bodies, progressive supranuclear palsy, multiple system atrophy
- secondary: drug-induced (dopamine antagonists), CVD, toxins, infection
131
Define Parkinson's disease.
common slowly progressive asymmetrical neurodegenerative disorder predominantly affecting elderly
132
What investigations are needed in epilepsy?
brain imaging - CT or MRI
EEG - brain waves, take 1hr, lying at rest with photic stimulation
systemic provocations
133
What is the mechanism of carbamazepine?
Voltage gated Na+ channel blocker on pre-synaptic membrane. Blocks the Na+ influx; reduces neuronal excitability and decreases the action potential.
134
With which anti-epileptic should you avoid alcohol and grapefruit juice?
carbamazepine
135
Describe the mechanism of action of sodium valporate.
Weak sodium ion channel blocker. Inhibitor of GABA degrading enzymes, increased GABA stops action potential.
136
Which anti-epileptics can increase risk of Stevens-Johnson syndrome?
sodium valporate
phenytoin
lamotrigine
137
How does lamotrigine work?
Varied mechanism of action. Inhibits voltage-gated Na+ channels and/or Ca2+ channels. Acts on pre-synaptic neuronal membrane, reduces action potential and excitatory signals.
138
Discuss the mechanism of action of Levetiracetam.
SV2A is a synaptic vesicle protein required for neurotransmitter release. Drug blocks this and reduced neurotransmitter release. Induces an anti-epileptic effect
139
What is the most common gene mutation that causes PD?
PARK8 (LRRK2) - 70% chance of developing PD
140
Look over clinical neuroanatomy lecture.
DON'T SKIP THIS!!
141
Which infectious syndromes do bacterial microbes give rise to in the CNS? Name the three most common pathogens.
- meningitis, meningo-encephalitis, abscess
| - meningococcus, pneumococcus, listeria
142
Which pathogens most commonly cause encephalitis as well as meningitis?
```
enterovirus
HSV
VZV
HIV
mumps
```
143
Cryptococcosis is an example of a fungal microbe. Which syndromes do these commonly lead to in the CNS?
meningo-encephalitis
| mass lesion
144
Which type of microbe is toxoplasmosis?
protozoal
145
What is meningitis? Differentiate between acute and sub-acute.
- inflammation of meninges
- acute: bacterial or viral
- sub-acute: bacterial (listeria, TB)
146
What are the signs and symptoms of meningitis?
- headache
- neck stiffness
- reduced GCS
- fever
- confusion (cerebritis/encephalitis)
- rash: purpuric and/or petechial but macular early on (meningococcal)
147
What are the risk factors for developing pneumococcal BM?
70% underlying disorder
- middle ear disease
- head injury
- neurosurgery
- alcohol
- immunosuppression (HIV)
148
Immunosuppression and pregnancy are risk factors to developing which type of BM?
listeria
149
What are some distinguishing factors of pneumococcal meningitis?
- focal signs
- seizures
- VIII palsy
- other pneumococcal infection signs e.g. endocarditis, CAP, ENT
150
List factors which are associated with poor prognosis in bacterial meningitis.
- pneumococcus
- reduced GCS
- CNS signs
- older age > 60yrs
- CN palsy (pneumococcal)
- bleeding (meningococcal)
151
What investigations would you undertake for suspected meningitis?
- history and exam (throat, cranial nerves)
- blood cultures and PCR
- throat culture, viral gargle
- FBC, UEs, LFTs, CRP
- lumbar puncture - cell count, gram stain, culture, PCR, protein, glucose, viral PCR
152
LP should routinely be performed before CT. When should CT be arrived out first?
- GCS < 12
- CNS signs
- papilloedema
- immunocompromised
- seizure
153
When is a lumbar puncture contraindicated?
- brain shift
- rapid GCS reduction
- resp/cardiac compromise
- severe sepsis
- rapidly evolving rash
- coagulopathy
154
Which antibiotic is first line therapy in possible bacterial meningitis?
IV ceftriaxone 2g 12hrly
155
Discuss the definitive antibiotic therapy for meningococcal, pneumococcal and listeria BM
- meningococcal: IV ceft or benpen 5 days
- pneumococcal: IV ceft or benpen 10-14 days
- listeria: IV amox (stop ceft) 21 days - increase if complications
156
Should corticosteroids be used in BM?
YES for proven BM
| 10mg QID dexamethasone 4 days
157
Discuss mechanisms put in place to prevent meningoccal infection. (5 points)
- primary: childhood immunisations - HIB, pneumo, mening
- secondary: chemoprophylaxis
- travel to high prevalence areas: ACWY
- asplenia, complement deficiency: men boosters, HIB and pneumo
- cochlear implants: pneumo booster
158
How is viral meningitis diagnosed and managed?
- only after exclusion of BM
| - consider aciclovir only if immunocompromised or confused (encephalitis)
159
How would you investigate viral encephalitis?
- history: confusion, fever, seizures
- lymphocytic CSF (normal glucose), PCR
- EEG
- MRI
160
Discuss the effects of intra-cerebral TB.
- sub-acute (weeks)
- may be unmasked during TB Rx
- CN lesions III, IV, VI, IX
161
How would you treat intra-cerebral TB?
- steroids
| - Rx for one year (RIF, INH, Pyraz, Etham)
162
How does HIV brain disease develop and in what ways does it manifest?
- unrecognised/untreated infection and marked immunodeficiency or lifestyle
- encephalitis
- dementia
- neuro-syphilis
- opportunistic
163
What is PMLE?
progressive focal multifocal leucoencephalopathy - progressive motor dysfunction
164
In which patients does PMLE develop?
immunocompromised, HIV, anti-TNF, transplant, JCV
165
Which pathogen commonly gives rise to intra-cerebral toxoplasmosis?
toxoplasma gondii
166
How does intra-cerebral toxoplasmosis manifest?
headache, seizures, focal CNS signs
167
How would investigate suspected intra-cerebral toxoplasmosis?
IgG and IgM - blood
| PCR - CSF
168
Which drugs are used in the treatment of toxoplasmosis?
sulphadiazine + pyramethamine
169
How is CSF investigated in cryptococcal meningitis?
india ink
cryptococcal antigen
culture
170
Amphotericin B and flucytosine are used in the treatment of which pathogen causing meningitis?
cryptococcal
