Neurology & Neurosurgery Flashcards
1
Q
Name the cells that produce myelin in
A) CNS
B) PNS
A
CNS = oligodendrocytes
PNS = Schwann cells
2
Q
Where in the brain is
A) Broca’s area
B) Wernicke’s area
A
Broca’s area = frontal lobe
Wernicke’s area = Posterior superior temporal lobe
3
Q
What is the function of
A) Broca’s area
B) Wernicke’s area
Also describe the aphasia of each region if they become damaged
A
A) Broca’s = production of speech – (damage causes non-fluent aphasia with word finding difficulties)
B) Wernicke’s = processing & understanding speech – (damage causes fluent aphasia, talks nonsense
4
Q
Which regions of the brain are responsible for
A) Visual processing
B) Auditory processing
A
A) Visual = parietal lobe
B) Auditory = Temporal lobe
5
Q
where are the cell bodies of motor nerves found?
A
Ventral horn
6
Q
where are the cell bodies of sensory nerves found?
A
Dorsal horn
7
Q
Explain the pathway of an upper and lower motor neurone (from CNS to muscle)
A
brain and brainstem -> ventral horn of the spinal cord (changes from upper to lower motor neurone here) -> peripheral muscles
8
Q
Describe the action of a parasympathetic neuromuscular junction
A
Ach ->
nicotinic receptor on postganglionic neuron ->
Ach ->
muscarinic receptor on target organ
9
Q
Describe the action of a sympathetic neuromuscular junction
A
Ach ->
nicotinic receptor on post ganglionic neuron ->
norepinephrine ->
adrenergic receptors on target organ
10
Q
Describe the findings in an upper motor neurone lesion
A
UPPER (everything is UP) – lesion is in brain or spinal cord (above level of ventral horn)
- Hyperreflexia
- Upgoing plantars
- Increased tone
11
Q
Where is an upper motor neurone lesion?
A
lesion is in brain or spinal cord (above level of ventral horn)
12
Q
Where is a lower motor neurone lesion?
A
Lesion is in peripheral nerves (below level of anterior horn)
13
Q
Describe the findings in a lower motor neurone lesion
A
LOWER (everything is down) –
- Reduced/absent reflexes
- Down going plantars/no response
- Reduced tone
- Muscle atrophy/fasciculations
14
Q
What function are the following spinal tracts responsible for
- The Corticospinal/ pyramidal tract
- The Posterior/ dorsal column
- The Lateral spinothalamic tract
A
15
Q
Describe the neurological findings in brown squared syndrome
A
Ipsilateral loss of fine touch, vibration, proprioception & motor
Contralateral Loss of pain & temp
16
Q
What causes brown squared syndrome?
A
Damage to half of the spinal cord
17
Q
Which type of fibres pick up proprioception
A
A-alpha (myelinated)
18
Q
Which type of fibres pick up ‘touch’
A
A-Beta (myelinated)
19
Q
Which type of fibres pick up sharp pain?
A
Unmyelinated C fibres (small and slow)
20
Q
Which type of fibres pick up dull pain?
A
Myelinated A-delta fibres (myelinated and fast)
21
Q
What is the definition of allodynia?
A
pain experienced with a sensory input that does not normally cause pain
22
Q
Explain the difference between chronic primary pain and chronic secondary pain and the way that they should be managed
A
Chronic primary pain = no underlying cause – DO NOT START PATIENTS ON PAIN MEDS (but u can start antidepressants)
Chronic secondary pain = underlying cause. Medications targeted to the underlying cause are fine
23
Q
State the type of medication each of the following are:
Amitriptyline
Duloxetine
Gabapentin and pregabalin
A
- Amitriptyline = tricyclic antidepressant
- Duloxetine = SNRI antidepressant
- Gabapentin & Pregabalin = anticonvulsant
24
Q
How is a breakthrough dose of morphine calculated?
A
Breakthrough dose = 1/6th of daily morphine dose
25
How is oral codeine/tramadol converted to oral morphine?
divide by 10
26
How is oral morphine dosing converted to subcutaneous morphine?
divide by 2
27
What is normal intracranial pressure?
7-15mm
28
What is Cushing's triad?
bradycardia, hypertension and irregular breathing
29
How is Cerebral perfusion pressure calculated?
Cerebral perfusion pressure (CPP) = Difference between mean arterial pressure (MAP) -intracranial pressure (ICP)
30
What are the functions of the following structures in relation to memory:
1. Hippocampus
2. Cortex
3. Thalamus
4. Limbic system
1. Hippocampus (forms memories)
2. Cortex (stores memories)
3. Thalamus (Searches and accesses memories)
4. Limbic system (adds emotion significance to events which helps in the formation of memory)
31
What is meant by integrate memory loss?
inability to form new memories
32
What is meant by retrograde memory loss?
inability to access old memories
33
What are the 4 main wave patterns seen on EEG?
Beta
Alpha
Theta
Delta
34
Explain the appearance of each wave and when you might see it
35
Describe the 4 stages of sleep and what waveform is seen in each
Stage 1- dozing. High amplitude, low frequency, slow theta waves.
Stage 2- regular sleep. Sleep spindles
Stage 3- deep sleep. High amplitude, very slow (2Hz) delta waves interspersed with short episodes of faster waves. Declining spindle activity
Stage 4- Very deep sleep. Delta waves
REM- low amplitude, high frequency (similar to the awake state)
36
When in the sleep cycle do sleep walking, sleep talking and night terrors occur?
Stage 4 (very deep sleep)
37
When in the sleep cycle do dreams and nightmares occur?
REM
38
When in the sleep cycle does REM occur?
Once the body reaches stage 4 sleep, the body then moves back up through stage 3 and stage 2 before entering REM sleep.
lasts 5-30 mins every 90 mins
39
Which stage in the sleep cycle do narcoleptics fall straight into?
REM
40
What is meningitis?
Infection/inflammation of the meninges
41
What is encephalitis?
Infection/inflammation of the brain
42
What is myelitis?
Infection/inflammation of the spinal cord
43
What is the most common bacterial cause of meningitis?
Neisseria Meningititis
44
What is the most common viral cause of meningitis?
Enteroviruses e.g. coxsackie
45
In which type of infection (bacterial/viral/fungal) would you see a fibrin web in the lumbar puncture?
Fungal
46
What glucose measurement would you expect in the CSF of a person infected with:
A) Bacteria
B) Virus
C) Fungus
A) Bacteria = <2.2 (low)
B) Virus = normal
C) Fungus = 1.6-2.5 (low)
47
What is the initial empirical treatment of meningitis in babies <3m?
IV cefotaxime + amox
48
What is the initial empirical treatment of meningitis in those aged 3M-50Y
IV cefataxime
49
What is the initial empirical treatment of meningitis in those >50Y?
IV cefotaxime + Amox
50
What is the initial empirical treatment of meningitis in those with meningococcal meningitis?
IV benzylpenicillin or cefotaxime
51
What is the initial empirical treatment of meningitis in those with meningitis caused by listeria?
IV amox + gent
52
What is the most common cause of encephalitis?
Herpes simplex
53
What are the 2 antibodies associated with autoimmune encephalitis?
Anti-VGKC and Anti-NMDA
54
What is the most common cause of brain abscess?
Strep
55
What are the 3 steps to manage rabies immediately post-exposure?
Wash wound
Give active rabies immunization
Give human rabies immunoglobulin (passive immunisation) if high risk
56
What is the preventative treatment for tetanus?
Inactivated tetanus vaccine
57
What is the treatment for tetanus after an exposure?
Penicillin
Immunoglobulin for high risk wounds/patients
58
What is the treatment for botulism?
Anti-toxin (A,B,E)
Penicillin / Metronidazole (prolonged treatment)
Radical wound debridement
59
What kind of organism causes Creutzfeldt-Jakob?
Prion
60
How is Creutzfeldt-Jakob diagnosed?
MRI, EEG, CSF
61
What is the treatment for Creutzfeldt-Jakob?
There is no treatment
62
What are the three main features of Wernicke's encephalopathy?
nystagmus
Opthalmaplegia
Ataxia
63
What are the features of Korsakoff's encephalopathy?
Wernicke's (nystagmus, opthalmaplegia, ataxia) +
Amnesia
Confabulation
64
What is confabulation?
gaps in memory are unconsciously filled with fabricated, misinterpreted, or distorted information
65
Describe the physical manifestations of a tonic clonic seizure
Rigid and shaking
66
Describe the physical manifestations of a tonic seizure
Stiffening
67
Describe the physical manifestations of an atonic seizure
Drop attacks
68
Describe the physical manifestations of a myoclonic seizure
Jump or jolt
69
Describe the physical manifestations of an absent seizure
Staring into space
70
Describe the physical manifestations of a partial/focal seizure
Rising feeling in stomach
Funny taste/ smell
Deja vu
Lip smacking
Repetitive picking at clothing
71
Where in the brain does a focal/partial seizure occur?
Temporal lobe
72
Describe the physical manifestations of an infantile spasm
Cyclical, repetitive full body spasming and relaxing
73
What is another name for infantile spasms?
West syndrome
74
Is the prognosis of west syndrome good or bad?
Bad
75
What are the treatments for tonic clonic, tonic and atonic seizures?
Men/women not able to get pregnant: Sodium valproate
Women able to get pregnant: Lamotrigine
76
What is the treatment for myoclonic seizures?
Men/women not able to get pregnant: Sodium valproate
Women able to get pregnant: Levetiracetam
77
What is the treatment for absent seizures?
Ethosuximide
78
What is the treatment for partial/ focal seizures?
Lamotragine
79
What is the treatment for west syndrome?
ACTH and Vibagatrin
80
What is 'status epileptics'?
seizure lasting >5 minutes or repeated seizures without regaining consciousness in between
81
What are the rules regarding driving after a first seizure with NORMAL investigations
Group 1 vehicles after 6 months
Group 2 (HGV) vehicles after 5 years
82
What are the rules regarding driving if you have a diagnosis of epilepsy?
Have been seizure free for one year
Have an established pattern of seizures only during sleep for at least 1 year
If awake seizures as well as sleep seizures, established pattern of only sleep seizures for three years
Should not drive during medication withdrawal and for 6 months thereafter
83
What is the definition of a primary headache vs a secondary headache?
Primary headache = no underlying medical cause. Caused by sensitisation of normal pain pathways
Secondary headache = underlying medical cause (e.g. meningitis)
84
What causes a postural headache?
Low pressure (e.g. CSF leak)
85
Describe the management of a tension headache (acute & preventative)
Acute: Paracetamol & NSAIDs
Preventative: Tricyclic antidepressants (amitriptyline)
86
Describe the management of a cluster headache (acute & preventative)
Acute: Nasal triptans, high flow oxygen,
Preventative: Verapamil
87
Describe the management of a migraine (acute & preventative)
Acute: NSAIDs, paracetamol, Triptans, anti-emetics
Preventative: trigger management, propranolol
88
Describe the management of a medication overuse headache
Withdraw medications
89
Describe the management of a sub arachnoid haemorrhage (diagnosis and management)
Diagnosis: CT Head as soon as possible
Lumbar Puncture > 12 hours after headache onset
Management: Clipping/coiling of aneurysms
Nimodipine (Ca2+ channel blocker for vasospasm)
90
Describe the management of raised ICP
Bed rest, fluids, analgesia, caffeine
Epidural blood patch (stiffens the meninges and helps symptoms)
91
Describe the management of a hormonal headache
Triptans and NSAIDs
92
Describe the management of giant cell arteritis (diagnosis and treatment)
Diagnosis: ESR & biopsy
Management: High dose prednisolone
93
Describe the management of trigeminal neuralgia
Management: carbamazepine
94
What is the mechanism of action of triptans?
5-HT receptor agonists
95
What scoring system can be use in A&E to assess the likelihood of a stroke?
ROSIER score in A&E (>1 = stroke likely)
96
What is the defining feature of a TIA?
<24hrs of symptoms
97
Describe the acute management of a TIA (5)
Exclude hypoglycaemia
Aspirin 300mg and
Referral to a specialist within 24 hours
Diffusion weighted MRI
Carotid doppler & ECG
98
Describe the acute management of ischaemic stroke
Exclude hypoglycaemia
CT Head
Thrombolysis: within 4.5 hours of stroke onset – Alteplase
Thrombectomy: within 24 hours of symptom onset in proximal anterior or posterior circulation strokes only (give thrombolysis alongside if <4.5 hrs)
99
What is the acceptable 'door to needle' time in a stroke?
30 mins
100
Describe the secondary prevention that patients who have suffered a stroke or a TIA should receive
Diet, exercise, stop smoking
Clopidogrel
Atorvastatin
BP and diabetes control
Warfarin (for AF) if applicable
Carotid endarterectomy if applicable
101
Describe the acute management of Intracerebral haemorrhage (haemorragic stroke)
CT Head
Blood pressure control
Reversal of anticoagulants (if relevant)
ICP control (Burr holes or craniotomy)
102
Describe the secondary prevention of Intracerebral haemorrhage (haemorragic stroke)
Manage hypertension
AVOID STATINS (unless benefit outweighs risk)
103
Describe the acute management of sub arachnoid haemorrhage
<6 hours = CT head (look for hyper-attenuation)
>12 hours = Lumbar puncture
Nimodipine to stop vasospasm
Blood pressure management (achieve >140mmHg)
Endovascular coiling
104
Describe the secondary prevention of sub arachnoid haemorrhage
BP control
Risk factor management
105
What is the function of the frontal lobe?
High level cognitive functions
Memory
Motor cortex (precentral gyrus)
106
What artery supplies the frontal Cortex?
Anterior cerebral artery
107
In which area of the brain can Broca's area be found?
Frontal cortex
108
What is the function of the parietal cortex?
Sensory cortex (touch, pressure and position- post central gyrus)
Self and spatial Awareness
109
Which artery supplies the parietal cortex?
Middle cerebral
110
what is the function of the occipital cortex?
Vision
111
Which artery supplies the occipital cortex?
Posterior communicating
112
Explain the blood supply of the motor and sensory cortexes
shared blood supply from anterior and middle communicating arteries.
Limb/facial weakness will be dependent on which artery is blocked and is distributed according to the image below.
113
What is a watershed region?
areas which lie between two areas with different arterial supplies
114
A stroke on which side of the brain will cause neglect and inability to recognise faces?
Right Hemisphere
115
Which vessel is blocked in a Total Anterior Circulation Stroke?
Carotid artery or middle cerebral artery
116
What are the criteria for a Total Anterior Circulation Stroke?
ALL 3
1. Unilateral weakness (with or without a sensory deficit) of the face, arm and leg
2. Loss of vision on one side (homonymous hemianopia)
3. Loss of awareness on one side (stroke on the non-dominant side of the brain causes you to totally ignore one side of the body) OR Dysphagia (stroke on the dominant side of the brain)
117
Which vessel is blocked in a partial Anterior Circulation Stroke?
one of the branches of the middle cerebral artery
118
What are the criteria for a partial Anterior Circulation Stroke?
2 out of 3 of the TACS criteria
119
Which vessel is blocked in a lacunar stroke?
blockage in a small artery in the brainstem, basal ganglia or subcortical area
120
What are the criteria for a Lacunar Stroke?
ONE of the following;
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis (weakness and uncontrolled movements on the same side of the body
121
Which vessel is blocked in a posterior circulation stroke?
a blockage in any of the posterior arteries
122
What are the criteria for a posterior circulation stroke?
a combination of symptoms including;
* Loss of balance/coordination
* Vertigo
* Double vision
* Dysarthria
* Visual loss
123
What does a basilar artery stroke cause?
Locked in syndrome
124
What is the name given to bruising over the mastoid?
Battles sign
125
What is battles sign indicative of?
a fracture in the petrous temporal bone which is leaking blood
126
What are the classical signs of shaken baby syndrome?
brain swelling
subdural haematoma
traumatic axonal injury
contusion tears.
127
For a subdural bleed, describe:
1. Shape on CT scan
2. Blood vessels affected
3. Usual mechanism of injury
4. Usual demographic affected
1. crescent
2. Sheared bridging veins
3. Fall
4. Elderly and alcoholic
128
For an extradural bleed, describe:
1. Shape on CT scan
2. Blood vessels affected
3. Usual mechanism of injury
4. How patients present
1. Lemon
2. Middle meningeal artery
3. Blow to pterion region
4. Lucid period then sudden collapse
129
What is Traumatic Diffuse Axonal Injury?
Injury to neurons caused by tearing in the white matter.
130
What causes Traumatic Diffuse Axonal Injury?
extensive brain movement (e.g, somebody being kicked in the head, falling from height, or road traffic accidents)
131
How is a diagnosis of Traumatic Diffuse Axonal Injury made?
Microscopically
132
What will happen to the patient immediately after Traumatic Diffuse Axonal Injury has occurred?
Immediately unconscious
133
What should doctors be suspicious of if a patient has a sudden change in personality/behaviour?
Frontal lobe tumour
134
What is the most malignant type of brain tumour?
Astrocytoma (e.g. glioblastoma)
135
what condition should be thought of in a patient with bilateral vestibular schwannomas?
neurofibromatosis II
136
Name 4 cancers that metastasise to the brain
- Breast
- Kidney
- Lung
- Skin
137
On which chromosome is the mutation that causes neurofibromatosis type 1?
Chromosome 17
138
What is the mode of inheritance in neurofibromatosis I?
Autosomal dominant
139
What does the gene involved in neurofibromatosis I usually code for?
neurofibromin (tumour suppressor)
140
What are the clinical signs and symptoms of neurofibromatosis I?
CRABBING
* Café au lait spots
* Relative with the condition
* Axillary or inguinal freckling
* Bony dysplasia (often Bowing of legs)
* Iris hamartomas
* Neurofibromas
* Glioma of optic pathways
141
On which chromosome is the mutation that causes neurofibromatosis type 2?
Chromosome 22
142
What is the mode of inheritance in neurofibromatosis 2?
Autosomal dominant
143
What does the gene involved in neurofibromatosis 2 usually code for?
merlin (tumour suppressor)
144
What is tuberous sclerosis?
Genetic condition in which benign tissue growths called hartomas grow and can affect multiple systems
145
What is the inheritance pattern of tuberous sclerosis?
Autosomal dominant
146
describe some of the findings a patient with tuberous sclerosis may exhibit
Ash leaf spots
shagreen patches
angiofibroma’s
ungual fibromas
café-au-lait spots
isolated white spots of hair/eyebrow/eyelashes/beard
147
What causes MS?
Autoimmune destruction of oligodendrocytes
148
What ocular signs and symptoms may be seen in a patient with MS?
Optic neuritis =
- Central scotoma
- Impaired colour vision
- Relative afferent pupillary defect
149
How is an episode of optic neuritis treated?
High dose steroids
150
Name the 4 different 'types' of MS
- Clinically isolated syndrome (first episode)
- Relaxing remitting
- primary progressive
- Secondary progressive (started relaxing remitting then became progressive)
151
Describe how MS is diagnosed
More than one episode/relapse in different parts of the nervous system with time between them.
Lumbar puncture
MRI
152
What CSF findings would you expect in MS?
* Oligoclonal (inflammatory) bands
* normal glucose and protein
* low white cell count
153
How are relapses of MS managed?
Methylprednisolone
154
What is the pathology of MND?
Degeneration of the nerve itself (not a demyelinating disease!)
155
What is the average life expectancy in MND?
18M-2Y
156
What is the most common type of MND?
ALS
157
Which nerves does ALS start in?
Peripheral
158
Name the type of MND that affects the muscles of talking and swallowing
Progressive bulbar palsy
159
What is the classic finding in the tongue of a patient with progressive bulbar palsy?
Walnut tongue
160
How is ALS diagnoses?
Diagnosis of exclusion
161
Which nerves are affected in MND, upper or lower?
MIX!
162
Name the drug that can be given to MND patients to slow the progression of the disease
Riluzole
163
Which imaging modality is the best for detecting spinal pathology?
MRI
164
In mixed vitamin B12 / folate deficiency, which one should be replaced first and why?
- Replace vitamin B12 before folate to avoid subacute degeneration of the spinals cord
165
What is Syringomyelia?
fluid in the spinal cord
166
How does syringiomyelia present?
causes cape, bilateral distribution of symptoms
167
What symptoms does autoimmune myositis cause?
acute or subacute weak & painful muscles
168
How is autoimmune myositis managed?
Immunosupressants
169
What is the difference between polymyositis and dermatomyositis?
Polymyositis =muscle inflammation
Dermatomyositis= skin and muscle inflammation
170
Which antibodies are associated with:
Polymyositis
Dermatomyositis
?
Polymyositis = Anti-PM/Scl autoantibodies
Dermatomyositis = Anti-TIF1-γ antibody
171
What causes myasthenia gravis?
Autoimmune - antibodies attack ACh receptors
172
What other pathology is associated with myasthenia gravis?
Thymoma
173
What is the classic clinic sign in myasthenia gravis?
Fatiguable muscles
174
How is myasthenia gravis diagnosed?
- Antibody tests (AChR)
- CT/MRI of thymus gland
- Edrophonium test
175
How is myasthenia gravis treated?
- Immunoglobulins/plasma exchange drugs
- Steroids (suppress the immune system)
- Pyridostigmine blocks the cholinesterase enzyme and stops breakdown of acetylcholine
176
What is a myasthenic crisis?
An acute worsening of symptoms often triggered by another illness
177
How is a myasthenic crisis managed?
IV immunoglobulins and plasmapheresis
178
What is lambert eaton syndrome?
Autoimmune production of antibodies against voltage gated calcium channels
179
What condition is Lambert-Eaton Syndrome usually secondary to?
paraneoplastic syndrome (SCLC)
180
How can Lambert-Eaton Syndrome be differentiated from myasthenia gravis?
LES = Muscle weakness improves with use (opposite of myasthenia gravis)
181
What causes Guillan-Barré syndrome?
Molecular mimicry; Campylobacter jejuni has antigens that look like proteins on peripheral neurons
182
Describe the disease pattern in Guillan-Barré syndrome
Acute, symmetrical, ascending weakness
183
How should Guillan-Barré syndrome be managed?
IV immunoglobulins
184
What is Charcot-marie tooth?
Genetic condition causing Myelin or axon dysfunction
185
What is the inheritance pattern of Charcot-marie tooth?
Autosomal dominant
186
Describe the signs and symptoms of charcot-marie tooth
muscle wasting (inverted champagne bottle legs)
weakness
reduced tendon reflexes
peripheral neuropathy
high foot arches
187
What are the causes of peripheral sensory loss (peripheral neuropathy)
A: Alcohol
B: B12 deficiency
C: Cancer & CKD
D: Diabetes & Drugs (amiodarone)
E: Every vasculitis
188
What helps to differentiate bells palsy from a stroke?
Bells palsy= forehead frozen
Stroke = forehead spared
189
How should bells palsy be managed
Pred if within 72 hours of symptoms.
Refer urgently if symptoms persist >3 weeks with no improvement
190
What causes Horner's syndrome?
apical lung tumour compressing the sympathetic nerves supplying the face
191
What is the classic symptom triad of Horner's syndrome?
Ptosis, miosis, Anhydrosis
192
What are the classic symptoms of a 3rd nerve palsy?
Down, out & ptosis
193
What do patients with a trochlear nerve palsy struggle to do?
Struggle to go down stairs
194
What happens to the uvula if a patient has a vagus nerve palsy?
- Uvula deviates towards normal side
195
What happens to the tongue if there is a hypoglossal nerve palsy?
Deviates to abnormal side
196
What causes bulbar palsy?
LOWER motor neuron lesions affecting CN IX-XII
197
What are the clinical findings in bulbar palsy
* A wasted, fasciculating tongue
* Dysarthria
* Dysphonia
* Dysphagia
198
What causes pseudo bulbar palsy?
UPPER motor neuron lesions affecting CN IX-XII
199
What are the clinical findings associated with pseudo bulbar palsy?
* Dysarthria (Disordered articulation & slurring of speech
* Dysphonia (A problem with the volume of their speech)
* Dysphagia (Difficulty swallowing)
* A spastic, immobile tongue
* A brisk jaw jerk
* A brisk gag reflex
200
What is the difference between bulbar palsy and pseudo bulbar palsy?
Bulbar = Caused by LOWER motor neuron lesions affecting CN IX-XII
Psuedobulbar = caused by UPPER motor neuron lesions affecting CN IX-XII
201
What colour should normal CSF be?
Clear/colourless
202
What is a normal specific gravity for CSF?
1.007
203
What is a normal pH for CSF?
7.33-7.35
204
Describe the flow of CSF
lateral ventricles ->
foramen of munro ->
third ventricle ->
cerebral aqueduct ->
fourth ventricle ->
Foramen of Luschka (lateral) or the Foramen of Megendie (medial) ->
circulate around the brain and spinal cord ->
Absorbed by arachnoid villi (granulations) that extend into the dural venous sinuses
205
What is spina bifida occulta?
Patch of hair and dimple - small gap in the spine, but no opening or sac on the back
206
What is spina bifida with a meningiocoele?
protruding bubble containing CSF
207
What is spina bifida with a Myelomeningiocoele
protruding bubble containing CSF and spinal nerves
208
Name the three types of delirium
- Hypoactive
- Hyperactive
- Mixed
209
Name 4 treatable causes of dementia
- Vitamin B12 Deficiency
- Thyroid Disease
- HIV & Syphilis
210
What causes Alzheimer's?
β-amyloid plaques and neurofibrillary tangles
211
What drugs can be given to help manage Alzheimer's?
Cholinesterase inhibitors (e.g. Donepezil, rivastigmine) - maintains acetylcholine which compensates for the loss of receptors
NMDA antagonist (memantine)
Cells in Alzheimer make too much glutamate (toxic), memantine blocks effects of glutamate
212
What is frontotemproal dementia also known as?
Picks disease
213
What causes frontotemporal dementia?
Tau pathology
214
What are the key features in frontotemporal dementia?
early change in personality / behaviour
215
How is frontotemporal dementia managed?
Supportive- no treatment available
216
What causes Lewy body dementia?
Lewy bodies (accumulations of α synuclein in the brain)
217
What are the key features of Lewy body dementia?
Fluctuation in symptoms
Visual hallucinations
Parkinsonisms
218
What is the key feature in vascular dementia?
Stepwise decline
219
describe the genetics behind Huntington's disease
CAG trinucleotide repeat in HTT gene on chromosome 4
220
What is meant by anticipation?
over generations the CAG repeat expands resulting in earlier onset and more severe disease
221
Describe the pathophysiology of Parkinson disease
Reduction of dopamine in the Substantia Nigra (part of basal ganglia)
222
Describe the clinical signs of parkinsons
Asymmetrical Stiffness
slow movements
change in posture
tremor (4-6 hertz)
223
How is parkinson's diagnosed?
Clinical diagnosis but can be graded with functional imaging
224
Describe the 4 main classes of parkinson's medication and briefly explain how they work
Levodopa – synthetic dopamine
COMT inhibitors (entacapone) - slows breakdown of levodopa (levodopa and COMT are given together)
Dopamine agonists (Bromocriptine, cabergoline) – Less effective than levodopa. Used to delay use of levodopa or used in tandem to facilitate a lower dose.
MAO-B inhibitors (selegiline) – Blocks the enzyme that breaks down dopamine
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How many hertz is a benign essential tremor?
6-12
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Is benign essential tremor symmetrical or asymmetrical?
Symmetrical
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is benign essential tremor better or worse with voluntary movement?
Better
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What happens to benign essential tremor when the patient is asleep or has been drinking alochol
it improves
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What medications can be given to help manage benign essential tremor?
propranolol or primidone
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What are the causes of Horner's syndrome?
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