Neurology Flashcards
1
Q
What is epilepsy?
A
Common neurological condition characterised by recurrent seizures
Epilepsy is not the only reason people have seizures
2
Q
What are febrile convulsions?
A
Typically occur in children between the ages of 6 months and 5 years
Around 3% will have at least one febrile convulsion
Usually occur early in a viral infection as the temperature rises rapidly
Seizures are typically brief and generalised tonic/tonic clonic in nature
3
Q
What are alcohol withdrawal seizures?
A
Occur in pts with a hx of alcohol excess who suddenly stop drinking ie
Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzos) and inhibits NMDA type glutamate receptors
Alcohol withdrawal leads to the opposite
Peak incidence of seizures is around 36 hrs following cessation of drinking
Pts are often given ben os following cessation of drinking to reduce the risk
4
Q
What are psychogenic non epileptic seizures?
A
Previously termed pseudoseizures, this term describes ots who present with epileptic like seizures but do not have characteristic electrical discharges
Pts may have hx of mental health problems or a personality disorder
5
Q
What are focal seizures?
A
Previously termed partial seizures
These start in a specific area, on one side of the brain
The level of awareness can vary in focal seizures
Focal aware of focal impaired
Further to this, focal seizures can be classified as being motor, non motor or having other features such as aura
6
Q
What happens in generalized seizures and what are the specific types?
A
Consciousness is lost immediately
The level of awareness classification is not needed
All patients lose consciousness
They can be subdivided into motor eg: tonic clonic and non motor (absence)
Specific types;
Tonic clonic (grand mal) Tonic Clonic Typical absence (petit mal) Myoclonic- brief, rapid muscle jerks Atonic
7
Q
What are infantile spasms (wests syndrome)?
A
Brief spasms beginning in the first few months of life
You get flexion of head, trunk, limbs —> extension of arms (salaam attack); last 1-3 secs, repeat up to 50 times
Progressive mental handicap
EEG; hypsarrythmia
Usually 2nd to serious neurological abnormality
Poor prognosis
8
Q
What is lennox gastaut syndrome?
A
May be extension of infantile spasms (50% have hx)
Onset 1-5 years
Atypical absences, falls, jerks
90% have moderate to severe mental handicap
EEG shows slow spike
Ketogenic diet may help
9
Q
What is juvenile myoclonic epilepsy?
A
Typical onset in the teens, more common in girls
1. Infrequent generalized seizures, often in morning
2. Daytime absences
3. Sudden, shock like myoclonic seizure
usually good response to sodium valproate
10
Q
What are the symptoms and signs of epilepsy?
A
Generalised seizures may bite their tongue and experience incontinence of urine
Asking about such features can be useful way of detecting epileptic seizures when taking a hx from a patient who presents with blackout or collapse
Following a seizure, pts typically have a postictal phase where they feel drowsy and tired for around 15 mins
11
Q
What IX do you do for seizures?
A
EEG and neuroimaging (MRI)
12
Q
How do you treat epilepsy?
A
Most neurologists now start antiepileptics following a second epileptic seizure…
As a general rule
Sodium valproate is used first line for pts with generalised seizures
Carbamazepine is used first line for pts with focal seizures
13
Q
What is the acute management of seizures?
A
Most seizures terminate spontaneously
When seizures don’t terminate after 5-10 mins then it is appropriate to administer medication to terminate the seizures
Benzodiazepines such as: diazepam are typically used and they may be administered rectally or intranasally/under the tongue
14
Q
What are the causes of UMN lesions?
A
Stroke
Tumour
Raised ICP
MS
15
Q
What is MS?
A
Multiple sclerosis (MS) is a chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system. This is caused by an inflammatory process involving the activation of immune cells against the myelin.
MS typically presents in young adults (under 50 years) and is more common in women. Symptoms tend to improve in pregnancy and in the postpartum period.
16
Q
What is charcots marie tooth?
A
Inherited disease that affects the peripheral motor and sensory nerves
They cause dysfunction in the myelin of the axons
Autosomal dominant
17
Q
What should you do with blood pressure in stroke?
A
Should not be lowered in the acute phase unless there are complications- hypertensive encephalopathy
18
Q
What should you do with regards to atrial fibrillation and anticoagulants in regards to stroke?
A
with regards to atrial fibrillation, the RCP state: ‘anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke’
19
Q
What is haemorrhagic transformation and what are the symptoms?
A
It is where an ischaemic stroke transforms into haemorrhagic stroke around 2 weeks after a stroke
The symptoms= confusion, one sided facial weakness and headache
20
Q
When should you start a statin after stroke?
A
if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation
21
Q
What are Cerebrovascular accidents?
A
Ischaemia or infarction of brain tissue secondary to inadequate blood supply
Intracranial haemorrhage
22
Q
What can cause a stroke?
A
Thrombus/embolus formation in patients with AF
Atherosclerosis
Shock
Vasculitis
23
Q
What is TIA?
A
Transient ischaemic attacks often precede a full stroke. A crescendo TIA is where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.
24
Q
What is the presentation of stroke?
A
In neurology, suspect a vascular cause where there is a sudden onset of neurological symptoms.
Stoke symptoms are typically asymmetrical:
Sudden weakness of limbs
Sudden facial weakness
Sudden onset dysphasia (speech disturbance)
Sudden onset visual or sensory loss
25
What are the risk factors for stroke?
```
Cardiovascular disease such as angina, myocardial infarction and peripheral vascular disease
Previous stroke or TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
Combined contraceptive pill
```
26
What is the immediate management for stroke?
Admit patients to a specialist stroke centre
Exclude hypoglycaemia
Immediate CT brain to exclude primary intracerebral haemorrhage
Aspirin 300mg stat (after the CT) and continued for 2 weeks
27
How do you manage TIA?
Start aspirin 300mg daily. Start secondary prevention measures for cardiovascular disease. They should be referred and seen within 24 hours by a stroke specialist.
28
What imaging is used once a stroke is diagnosed?
The aim of imaging is to establish the vascular territory that is affected. It is guided by specialist assessment.
Diffusion-weighted MRI is the gold standard imaging technique. CT is an alternative.
Carotid ultrasound can be used to assess for carotid stenosis. Endarterectomy to remove plaques or carotid stenting to widen the lumen should be considered if there is carotid stenosis.
29
What is the secondary prevention of stroke?
Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily)
Atorvastatin 80mg should be started but not immediately
Carotid endarterectomy or stenting in patients with carotid artery disease
Treat modifiable risk factors such as hypertension and diabetes
30
What type of dementia is motor neurone associated with?
Frontotemporal dementia
31
What is motor neurone disease?
Neurological condition of unknown cause which can present with both upper and lower motor neurone signs. It rarely presents before 40 years and thee are various patterns of disease- amyotrophic lateral sclerosis most common.
32
What are the features of motor neurone disease?
Fasciculations
The absence of sensory signs and symptoms
Mixture of lower motor neurone and upper motor neurone signs
Wasting of the small hand muscles, tibialis anterior is common
33
How can you diagnose motor neurone disease?
It is a clinical diagnosis
Nerve conduction studies will be normal and hep exclude a neuropathy
Electromyography shows a reduced number of action potentials and increased amplitude
34
What are the features of temporal lobe seizures?
Hallucinations (auditory/gustatory/olfactory), Epigastric rising/Emotional, Automatisms (lip smacking/grabbing/plucking), Deja vu/Dysphasia post-ictal)
35
What is the symptoms of frontal lobe seizures?
Head/leg movements, posturing, post-ictal weakness, Jacksonian march
36
What are the features of parietal lobe epilepsy?
Paraesthesia
37
What are the features of occipital lobe seizures?
Floaters and flashes
38
What is Myaesthenia Gravis?
Auto immune disease characterised by antibodies against the nicotinic acetylcholine receptors on muscle fibres
This limits the ability of acetylcholine to cause muscle contraction
39
What are the clinical features of myaesthenia gravis?
Weakness affecting limb musclds
Extra ocular muscles (drooping eyelids, diplopia), facial muscles (difficulty smiling or chewing)
Bulbar muscles (change in speech or difficulty swallowing)
On examination there may be fatiguable muscle weakness, bilateral ptosis, myaesthenic snarl, head drop, bulbar features- nasal speech, dysarthria, dysphagia
40
What are the investigations done for myaesthenia gravis?
Blood tests for serum acetylcholine receptor antibody
Muscle specific tyrosine kinase antibodies
CT chest to look for thymoma
Repetitive nerce stimulation (fall in muscle action potential between 1st and 4th action potential)
41
What extra test is done during a myaesthenic crisis?
Serial pulmonary function tests (spirometry) should be carried out
If Forced vital capacity is 15mL/kg or less then the pt should be considered for mechanical ventilation
42
What id the management of myaesthenia gravis?
Regular review and involvement of MDT' OT/PT/SALT
Medical management is with immunosuppressive agents (steroids given acutely) and anticholinesterase inhibitors (neostigmine/pyridostigmine) these inhibit the breakdown of acefglcholine
Thymectomy is considered in some pts
43
What are the SES of anticholinesterase inhibitors?
Salivation
Lacrimation
Diarrhoea
Urinary frequency
44
What is the first line treatment of focal seizures?
Lamotrigine or carbamazepine
45
What is status epilepticus?
Any seizure which lasts more than 5 minutes or if the pstient experiences more than one seizure and does not regain consciousness between the two.
46
What is the management of status epilepticus?
A-E
Oxygen
IV access
ABG
Glucose, FBC, UES, CRP Calcium phosphate and magnesium if the patient is on anti epileptics
Anaesthetic review to ensure airway is managef
IV lorazepam 4mg (second dose can be given if no response)
In the absencd of IV access then PR diazepam or buccal midazolam can br given
If initial benzos fail;
Leviteracetam
Phenytoin
Valproate
If seizures continue then intubation and general anaesthesia is necessary
47
What is wernickes encephalopathy?
What are the clinical features
What is the treatment
Wernickes encephalopathy is due to thiamine (B1 deficiency)
This can be caused by; chronic alcohol abuse, malnutrition, bariatric surgery, hyperemesis gravidarum
Clinical features= nystagmus, broad based gait
Triad= ataxia, confusion and ocular abnormalities
Treatment= IV pabrinex
Left untreated if can become korsakoffs
48
What is a total anterior circulation infarct defined by?
```
Contralateral hemiplegia/hemiparesis
AND
Contralateral honomunous hemianopia
AND
Higher cerebral dysfunction (aphadia, neglect)
```
A TACI involves the antetior AND middle cerebral arteries on the affected sign
49
What is a partial anterior circulation infarct defined by?
2 of
Contralateral hemiplegia/hemiparesis
Contralateral honomynous hemianopia
Higher cerebral dysfunction
OR
Higher cerebral dysfunction alone
PACI involves the anterior OR middle cerebral artery on the affectdd side
50
What is a lacunar infarct?
Pure motor stroke
Pure sensort sfrike
Sensiromotor stroke
Ataxic hemiparesis
There is no visual field defect, higher cerebral dysfuctiin, brainstem dysfunction
A LACI affects the small deep perforating arteries, typically supplying the internal capsule or thalamus
51
What are the signs of posterior infarct?
```
Nystagmus
Vertigo
Ipsilateral Horner’s syndrome
Ipsilateral facial sensory loss
Dysarthria & dysphagia
Diplopia
Dysarthria & dysphagia
Contralateral pain and temperature loss
```
52
what are the causes of foot drop?
weakness or paralysis of dorsiflexion and eversion
L5 root lesion (Radiculopathy)- also have sensory loss over the L5 dermaotype, sciatic burning type pain
Distal motor neuropathy- glove and stocking sesnroy disturbance and loss of all movements of the foot
Small cortical lesions
Uncommonly- intrinsic cord disease, partial sciatic nerve disease and myopathy
53
What are fasciculations a characteristic of?
motor neurone disease
54
what is bulbar palsy?
this is a lower motor neurone lesion affecting cranial nerves 9,10,12 and it causes impairments in speech and swallowing
You get absent or normal jaw jerk reflex, an absent gag reflex, a flaccid fasciculation tongue, nasal quiet speech, and signs suggestive of the cause- limb fasciculations in lower motor neurone disease
CAUSES- MND, BRAINSTEM STROKE, MYAESTHENIA GRAVIS, GBS
55
How do you treat cluster headaches?
Nasal sumatriptan helps relief the cluster headache
| verapamil is used for prevention
56
What is multiple sclerosis?
Disease predominantly affecting females
the aetiology is unknown
plaques of demyelination and eventual axonal loss are the radiological and pathological hallmark of the disease
It can either be relapsing remiting or primary progressive
57
What are the clinical features of MS?
MS is a disease of the central nervous system and therefore patterns of weakness or sensory loss that suggests a peripheral lesion are not consistent
Sensory disease (patchy paraesthesia)
Optic neuritis (loss of central vision and painful eye movements)
Internuclear opthalmoplegoa
58
What Ix would you do for MS?
Clinical Hx/exam
Imaging findings- periventricular white matter lesions seen on MRI
Oligoclonal bands in the CSF
59
How do you treat Multiple sclerosis?
An acute attack of multiple sclerosis should be treated with glucocorticoids- IV methylpred every 24 hours for 3 days
Severe acute attacks who do not respond to glucocorticoids should be covered with plasma exhange
```
Chronically....
Physio
Baclofen for spasticity
Modafininl and exercise therapy for fatigue
Anticholinergics for bladder dysfunction
SSRIs for depression
Clonazepam for tremor
```
60
What is the hallmark diagnostic test for GBS?
Raised protein with normal WCC on a lumbar puncture
61
What is GBS?
Ascending inflammatory demyelinating polyneuropathy
62
What are the causes of GBS?
Typically occurs 1-3 weeks after infection
Eg: campylobacter, mycoplasma, EBV
40% are idiopathic
63
What are the clinical features of GBS?
Progressive ascending symmetrical limb weakness (Affecting the lower limbs first)
Paraesthesia may precede the onset of motor symptoms
Resp muscles can be affected in severe cases
Some cases present with symptoms of cranial nerve palsies- diplopia, facial droop
64
How do you manage GBS?
Conservative measures include monitoring of ventilation w/ serial spirometry and ABG +/- ventilation
Also the need to carry out measures to reduce the risk of a VTE (TEDS, LMWH)
Protection of pressure areas
Medical management with IV immunoglobulin and if ineffective then plasmapheresis
65
What is the prophylaxis for migraines?
Propanolol or TOPIRAMATE in those where propanolol is contraindicated (Asthmatics)
66
What is parkinsons disease?
destruction of dopaminergic cells
67
what are the core features of parkinsons disease?
Bradykinesia
3-5Hz resting tremor
Lead pipe rigidity
These features combine together to give the phenomenon known as cogwheeling (a jerkiness felt when testing pts tone)
Parkinsonian gait
Hypomimic facies
Postural instability
68
What are the key features of parkinsoniam gait?
Small, shuffling steps, slowness of movement (especially on initiation and turning). flexed posture, assymetric tremor
69
What is a cluster headache?
Presentation?
Treatment?
The name of cluster headaches comes from the pattern, so cluster headaches typically occur in clusters lasting several weeks , with the clusters themselves typically once a year.
So cluster headaches last for 4-12 weeks and occur once or twice a day for 15mins- 2 hours
Intense, sharp stabbing pain around one eye
Pt is restless and agitated during the attack
redness, lacrimation, eyelid swelling, blocked nose
Treatment
In an acute case= 100% oxygen, subcut triptan
Prophylaxis= verapamil
69
What is a cluster headache?
Presentation?
Treatment?
The name of cluster headaches comes from the pattern, so cluster headaches typically occur in clusters lasting several weeks , with the clusters themselves typically once a year.
So cluster headaches last for 4-12 weeks and occur once or twice a day for 15mins- 2 hours
Intense, sharp stabbing pain around one eye
Pt is restless and agitated during the attack
redness, lacrimation, eyelid swelling, blocked nose
Treatment
In an acute case= 100% oxygen, subcut triptan
Prophylaxis= verapamil
70
What is the treatment plan for status epilepticus?
abc- airway adjunct, oxygen, check blood glucose
First line drugs= benzodiazepines ie: diazepam, lorazepam
In the prehospital setting diazepam may be given rectally, in hospital IV lorazepam is generally used, this may be repeated once after 10-20 minutes
If ongoing status it is appropriate to start a second line agent ie: phenytoin/phenobarbital
If no response (Refractory status) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia.
71
What is the management of Parkinson's disease?
If the motor symptoms are affecting a patients quality of life- Levodopa
If motor symptoms are not affecting a patients quality of life- Dopamine
72
What happens if a patient does not take their Parkinson medication?
Neuroleptic malignant syndrome- fever, severe muscle rigidity, altered consciousness, autonomic instability, dilated pupils
Akinesia (absence of movement)
73
What are the side effects of levodopa?
```
Anorexia
Unwanted movements
dry mouth
postural hypotension
psychosis
drowsiness
```
74
What is an example of a dopamine receptor agonist
| What are the side effects
Bromocriptine, ropinirole
| SEs; impulse control disorders and excessive daytime somnolence
75
What are the risk factors for stroke?
```
CVD- angina, MI, perioheral vascular disease
Previous stroke or TIA
Atrial fibrillation
Carotid atery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
COCP
```
76
How do you manage stroke?
Admit patients to a specialist stroke centre
Exclude hypoglycaemia
Immediate CT brain to exclude haemorrhage
Aspirin 300mg stat after the CT and continued for 2 weeks
Thrombolysis with alteplase can be used sfter CT brain scan has excluded intracranial haemorrhage
Needs to be given within 4.5 hours
77
What imaging is done to determine the vascular territory that is affected in a stroke?
Diffusion weighted MRI (CT= alternative)
Carotid ultrasound is used to assess carotid stenosis, endarterectomy to remove plaques or carotid stenting can be done if there is carotid stenosis.
78
What is the secondary prevention of stroke?
Atorvastatin but not immediately
Clopidogrel 75mg once daily
Carotid endarteectomy or stenting
79
What are the symptoms of an intracranial bleed?
```
Sudden onset headache
Seizures
Reduced GCS
Weakness
Vomiting
```
80
What is a subdural haemorrhage caused by?
Rupture of the bridging veins in the outermost meningeal layer
81
What is an extradural haemorrhage caused by?
Rupture of the middle meningeal artery in the temporo parietal region
Typical history is young person with ongoing headache
82
What are the principles of management of intracranial bleeds?
Immediate CT head to establish the diagnosis
Check FBC and clotting
Admit to a specialist stroke unit
Discuss with a specialist neurosurgical centre to consider surgical treatment
Consider intubation, ventilation and ICU care if they have reduced consciousness
Correct any clotting abnormality
Correct severe hypertension but avoid hypotension
83
What is the cause of subarachnoid haemorrhage?
Ruptured cerebral aneurysm
84
What are the features of SAH?
```
Thunderclap headache
Neck stiffness
Photophobia
Vision changes
Speech changes, weakness, seisures, loss of consciousness
```
85
What investigations done for SAH?
CT head is first line
Lumbar puncture is used to collect a CSF if the CT head is negative
CSF on LP of SAH will have xanthochromianand red cell count will be raised
Angiography can be used once the SAH is confirmed to locate bleeding source
86
What is the management of SAH?
Specialist neurosurgical unit
Sirgical intervention- coiling, clipping
Nimodipine- prevents vasospasm
87
What is MS?
Chronic and progressive condition which involves demyelination of the myelinated neurones in the CNS
It is caused by an inflammatory process causing immune cell activation againsg the myelin
88
What are the causes of MS?
Multiple genes
EBV
Low vitamin D
Smoking obesity
89
What are the symptoms of MS?
Optic neuritis (demyelination and loss of vision in one eye)
Eye movement abnormalities (sixth cranial nerve- abducens nerve) - internuclear opthalmoplegia and conjugate lateral gaze disorder
Focal weakness= Bells palsy, horners syndrome, limb paralysis, incontinence
Focal sensory symptoms= numbness, paraesthesia, trigeminal neuralbia, lhermittes sign (electric shock sensation that travels down the spine and into the limbs when flexing the neck)
Ataxia (can be sensory- loss of proprioception) or cerebellar (problems with co ordinating movement)
90
What are the disease patterns of MS?
Relapsing remitting
Primary progressive
Secondary progressive
91
What investigations can support the diagnosis of MS?
So diagnosis is normally made by a neurologist based on the clinical picture and symptoms suggesting lesions that change location over time.
Investigations can be done to support the diagnosis…
- MRI scans can demonstrate typical lesions
- lumbar puncture can detect oligoclonal bands in the CSF
92
How does optic neuritis present?
Central scotoma. This is an enlarged blind spot.
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect
93
Other than MS, what are the other causes of optic neuritis?
```
Sarcoidosis
Systemic lupus erythematosus
Diabetes
Syphilis
Measles
Mumps
Lyme disease
```
94
How is optic neuritis treated?
Patients presenting with acute loss of vision should be seen urgently by an ophthalmologist for assessment. It is treated with steroids and recovery takes 2-6 weeks. Around 50% of patients with a single episode of optic neuritis will go on to develop MS over the next 15 years. Changes on an MRI scan help to predict which patients will go on to develop MS.
95
What is the treatment of MS?
Treatment with disease-modifying drugs and biologic therapy has changed the management of multiple sclerosis so that the aim of treatment is now to induce long term remission with no evidence of disease activity. There are many options that target various mechanisms such as interleukins, inflammatory cytokines and various immune cells. Going into detail about these drugs is beyond what would be expected in your exams. Disease-modifying drug treatment will be coordinated by specialists in multiple sclerosis.
Treating Relapses
Relapses can be treated with steroids. NICE recommend methylprednisolone:
500mg orally daily for 5 days
1g intravenously daily for 3–5 days where oral treatment has failed previously or where relapses are severe
Symptomatic Treatments
It is important to treat the symptom that result from the disease process along with treating the disease process itself:
Exercise to maintain activity and strength
Neuropathic pain can be managed with medication such as amitriptyline or gabapentin
Depression can be managed with antidepressants such as SSRIs
Urge incontinence can be managed with anticholinergic medications such as tolterodine or oxybutynin (although be aware these can cause or worsen cognitive impairment)
Spasticity can be managed with baclofen, gabapentin and physiotherapy
96
What is motor neurone disease?
It is an umbrella disease which encompasses a variety of diagnoses
It is ultimately fatal and the moror neurones stop functioning, there is no effect on sensory neurones and patients should not experience sensory symptoms.
97
What are the 2 main complications of subarachnoid haemorrhages?
Vasospasm (can prevent this by giving nimodipine- CCB)
Hyponatraemia
98
What is the difference between a total anterior circulatory stroke (TACS) and partial anterior circulatory stroke (PACs)?
TACS: 3 of
Unilateral hemiparesis/ hemiplegia
Higher cortical dysfunction- dysphasia
Homonymous hemianopia
PACS: 2 of the above
99
What does a lacunar stroke present like?
Pure sensory stroke
Pure motor stroke
Sensori- motor stroke
Ataxic hemiparesis
100
What does posterior circulation syndrome stroke look like?
One of the following…
Cranial nerve palsy and a contralateral motor/sensory deficit
Conjugate eye movement disorder (gaze palsy)
Cerebellar dysfunction- ataxia, nystagmus, vertigo
Isolated honomynous hemianopia or cortical blindness
101
What is the scoring system for TIA?
ABCD2
102
What are the features of a cluster headache?
Unilateral
Lasts 15 mins- 3 hours
Retro orbital
Autonomic symptoms- lacrimation, red eye, excess tearing
Restless and want to move about
Ptosis/ miosis (can resemble horners)
Made worse by alcohol, often at the same time each day
103
What is the cluster headache treatment?
Acute attack: high flow 100% oxygen
Subcut sumatriptan
Preventative: verapamil or lithium
104
How do you treat status epilepticus?
Status epilepticus is where there is continous seizures for 5 minutes or no recovery in between episodes
Get IV access, A to E, check glucose level
Give IV lorazepam 4mg
If lorazepam does not work then give IV phenytoin 25mg/kg, anaesthetic guidance is needed
If phenytoin doesn’t work then try phenobarbital and ITU care
105
What are the difference between features of UMN and LMN?
UMN= no muscle wasting, clonus, hypertonia, brisk/normal reflexes, spasticity
LMN= muscle wasting, fasciculations, hypotonia, dominished/absent reflexes
106
What is hydrocephalus and what are the causes?
Enlargement of the ventricles
Can be obstructive or communicating
```
Obstructive= tumours, brain bleeds, cysts
Communicating= SAH, meningitis
```
107
How do you treat hydrocephalus?
VP shunt
108
What are the features of hydrocephalus in children?
Enlarged head circumference
Dilated scalp veins
Bulging anterior fontanelle
109
Why do you give dexamethasone in meningitis?
This is to prevent sensironeural hearing loss
110
How are CNS tumours graded?
Who grading
111
Give examples of CNS tumours…
Malignant- glioblastoma multiforme, medulloblastoma
Benign- meningioma, pituitary adenoma (adult), vestibular schwannoma (adult)
112
CNS tumours are mostly due to extra cranial mets, what are the 3 most likely mets to go to CNS?
Bowel
Lung
Breast
113
What are the signs of CNS tumour?
Fast growing= headaches, nausea
| Slow growing= neuro sx
114
What should you think of when a patient has bilateral acoustic neuromas?
Neurofibromatosis 2
115
What is bells palsy?
What are the risk factors?
How does it present?
How do you treat?
Facial nerve palsy- LMN lesion
Risk factors- URTI, pregnancy, DM, HTN, immunosuppression
Facial paralysis, hyperacusis
Steroids (within 72 hours), really important to look after the eyes- giving eye drops and taping close the lid
116
How do you work out GCS?
E4 V5 M6
```
Eye movement=
4= spontaneous
3= to speech
2= to pain
1= no response
```
```
V= best verbal response
5= orientated to time, place, person
4= confused
3= inapropriate words
2= incomprehensible sounds
1= no response
```
```
Motor
6= obeys command
5= moves to localised pain
4= flexion withdrawal (from pain)
3= abnormal flexion
2= abnormal extension
1= no response
```
117
What is PD?
Chronic neurodegenerative movement disorder caused by depletion of the dopaminergic neurons in the substantia nigra
This affects the basal ganglia and movement
118
What are the main clinical features of parkinsons disease?
Tremor
Rigidity
Bradykinesia
Postural instability
119
What would you see on examination in someone with parkinsons disease?
Gait- difficulty initiating movements, shuffling gait, freezing, difficulty turning, reduced arm swing
Unilateral redting tremor (pill rolling 4-6 Hz), mask like face (hypomimia)
Motor- rigidity (cogwheeling) power and reflexes may be normal
Micrographia- progressively smaller writing
120
What are the differentials for parkinsons disease?
Drug induced parkinsonism
Parkinson plus syndromes;
Multiple systems atrophy
Progressive supranuclear palsy
Lewy body dementia
121
What are the common drugs which cause drug induced parkinsonism ( second most common cause of parkinsonism after idiopathic PD)?
Think of the drugs which affect dopamine!
Typical antipsychotics- chlorpromazine, haloperidol
Atypical antipsychotics- risperidone, onlanzapine, aripiprazole
Antiemetics- metoclopramide
These drugs cause acute dystonia, tardive dyskinesia, akathisia
122
What are the sx pf multiple systems atrophy?
Autonomic sx (postural hypotension, constipation, sexual dysfunction, early falls, cerebellar involve,ent)
123
What sx would you get with progressive supranuclear palsy?
Vertical gaze palsy (wouldnt be able to look up)
| Early falls
124
What is the management of Parkinsons?
MDT approach
Neurology, SALT (really helpful in speech and language), physotherapy, occupational therapy, dietetics, community nursing, urology, mental health services
Parkinsons UK
125
What is the management of parkinsons disease?
First line: levodopa
Levodopa is usually given with dopa decarboxylase inhibitor- co careldopa and co beneldopa
Dopa decarboxylase inhibitors are needed as they prevent the conversion of levodopa in the peripheries, therefore increasing the amount in the CNS
126
What other drug options are there other than levodopa in PD?
What are the side effects?
Oral monoamine oxidase B inhibitos- selegiline, rasagiline
Oral dopamine agonists- pramipexole, ropinirole
Side effects= excessive sleepiness, hallucinations, impulse control disorders
127
How does benign essential tremor differ from PD tremor?
Benign essential tremor is symettrical and slightly faster than PD (5-8Hx)
Improves with rest and alcohol
Worsens with intentional ,ove,ent
128
What is MS?
An acquired, chronic, immune (T cell) mediated, inflammatory myelinating disorder of the CNS
It is characterised by 2 or more white matter lexions seperated in time and space
129
What are the clinical features of MS?
```
Lots of different ways of presenting
Unilateral visual deficit- optic neuritis
Double vision
Limb weakness
Gait ataxia
Bowel or bladder involvement
Sensory disturbance and more
```
130
What are the features of optic neuritis?
It is a partial or total visual loss which develops over hours to days
Eye pain is exacerbated by movement, they may have reduced colour vision
Central scotoma (obscuration of central vision)
On fundoscopy it may show a pale swollen optic disc
RAPD may be present
131
What is transverse myelitis in terms of MS?
Focal inflammation in the spinal cord causing weakness or sensory symptoms below the level of the lesion
132
What are the features of transverse myelitis in MS?
Lhermittes phenomena= electric shock like sensation which radiates down the spine and is induced by neck flexion
Urinary symptoms= frequency, urgency or retention
