Neurology Flashcards
1
Q
Define epilepsy
A
- Tendency to have recurrent, unprovoked seizures
- Seizure is transient excessive electrical activity with motor, sensory or cognitive manifestations
Epilepsy is defined by
- At least two unprovoked or reflex seizures occuring more than 24 hours apart
- One unprovoked seizure with probability of further seizures
- Diagnosis of an epilepsy syndrome
2
Q
List types of seizures
A
- Generalised, affecting the whole brain (tonic clonic, absence, atonic, tonic or rigid, clonic or convusive, myoclonic)
- Partial, affecting a focal part of the brain (simple, where consciousness is unimpaired, or complex where the consciousness is impaired)
3
Q
List symptoms of cauda equina syndrome
A
- Increasing backpain
- Bilateral sciatica
- Sensory loss in a lumbosacral distribution
- Flaccid, weakened lower limbs with reduced reflexes
- Indicates a neurosurgical emergency.
- Urinary symptoms, the anal sphincter is also likely to be involved
- Gait disturbance
- Erectile dysfunction
4
Q
List causes of cauda equina syndrome
A
- Bony metastasis
- Myeloma
- Epidural abscess
- Disc prolapse
- Epidural haematoma
- Primary sacral tumour e.g. chordoma
5
Q
How is cauda equina syndrome treated?
A
- Urgent same day referral to surgeon
- Imaging
- Surgical decompression
6
Q
List adverse effects of carbamezapine
A
- Sedation
- Nausea
- Diarrhea
- Rash
- Leukopenia
- Hyponatremia
7
Q
Define stroke
A
Focal neurological deficit lasting more than 24 hours if not interviened
8
Q
List types of stroke
A
- Ischaemic (embolus, thrombus formation 80%)
- Haemorrhagic (burst aneurysm, 20%)
9
Q
List risk factors of stroke
A
- Ischaemic heart disease
- Hypertension
- Atrial fibrillation
- Hypercholesterolaemia
- Diabetes
- Previous stroke or TIA
- Smoking
- Excessive alcohol intake
- Hypercoagulable disease (e.g. sickle cell anaemia, polycythemia vera)
- Prosthetic heart valves
- Carotid stenosis
- Poor ventricular function
- Migraine with aura
- Combined oral contraceptive pill
- Family history of stroke in first-degree relatives
10
Q
List investigations of stroke
A
- FBC
- CRP
- Lactate
- Clotting screen
- ECG (AF)
- Patent foramen ovale screen
- MDT (SALT, physio)
- Head CT (haemorrhagic stroke appears white, while ischaemic stroke appears darker due to loss of density following swelling and bursting of cells. White dot may represent a clot)
- ct angiogram for clot identification
- Carotid Doppler
11
Q
Describe treatment of ischaemic stroke
A
< 4.5 hours
- CT: no haemorrhage
- Thrombolysis (if no contraindications) using alteplase 10% as bolus then the rest over 1 hour
> 4.5 hours
- CT head (exclude haemorrhage)
- Aspirin (300mg), Swallow assessment
- Thrombectomy within 6 hours
- Maintain hydration, oxygenations, monitor glc
Secondary prevention
- Warfarin prophylaxis for AF patients
- Non-AF continue aspirin for 2 weeks then switch to lifelong clopidogrel
12
Q
Describe epidemiology of stroke
A
- In the UK, first ever stroke occurs in about 230/100,000 people per year and first-ever TIA in about 50/100,000 people per year.
- Stroke is the fourth single cause of mortality in the UK
13
Q
Define migraine
A
- Recurrent episodes of a headache lasting 4-72 hours
- Chronic
- Severe effect on quality of life
14
Q
Describe risk factors for migraine
A
- Skipping meals.
- Too much or too little sleep.
- Stressful events.
- Smoking.
- Depression or anxiety.
- Drinking too much alcohol, dehydration
- Loud or sudden noises.
- Caffeine, cheese, chocolate
- Menstruation
- Bright lights
- Family history
- Overuse of headache medication
- Obesity
- Female
- Allergies or asthma
- Hypertension
- Hypothyroidism
15
Q
List symptoms of migraine
A
- Unilateral headache (bilateral in children) lasting 4 to 72 hours if untreated
- Pulsating, throbbing, banging, pounding
- Aggravated by routine activities of daily living
- Nausea and or vomiting
- Photophobia
- Phonophobia
- Aura (visual, sensory, speech or language symptoms, atypical)
- Decreased ability to function
- Sensitivity to noise
- Aura
SULTANS - Severe unilateral throbbing activity impairing nausea and vomiting sensitivity to light and sound
16
Q
Describe treatment of migraine
A
Acute episodes - A and E
- Metclopramide or prochorperazine + diphenhydramine
- OR Sumatriptan OR promethazine OR valproid acid OR paracetamol OR magnesium sulfate
- (Antiemetic)
- Oxygen
- IV corticosteroid and secobarbital
Mild symptoms
- NSAID
- Antiemetic
- Hydration
- OR paracetamol
Severe symptoms
- Triptan
- Antiemetic
- Hydration
- NSAID
Avoid triggers
Prophylaxis
- Propanolol
- Amitriptyline
- Tropicamate
- Triptin
17
Q
Define tension headache
A
Mild to moderate intensity headache which can last minutes to days and is not aggravated by routine physical activity such as walking.
18
Q
List types of tension headache
A
- Infrequent episodic tension-type headache — less than one day of headache per month.
- Frequent episodic tension-type headache — at least 10 episodes of headache occurring on average 1–14 days per month for more than 3 months.
- Chronic tension-type headache — 15 or more days of headache per month for 3 or more months.
19
Q
List symptoms and signs of tension headache
A
- Generalised headache across the whole head usually described as a pressure or tightness around the head which often spreads into or arises from the neck.
- Mild to moderate intensity headache which can last minutes to days and is not aggravated by routine physical activity such as walking.
- Pericranial tenderness which may be elicited on manual palpation
- Normal neurological exam
20
Q
Describe management of tension headache
A
- Simple analgesia such as paracetamol, aspirin or nonsteroidal anti-inflammatories
- Avoidance of opioids.
- Identification and appropriate management of associated co-morbidities such as mood disorders, chronic pain and sleep disorders.
- Provision of patient information on tension-type headache and avoidance of medication overuse headache.
- Headache diary
Preventative treatments that may be considered for chronic tension-type headache include:
- A course of up to 10 sessions of acupuncture over 5–8weeks.
- Low dose amitriptyline (off-label indication).
21
Q
Describe aetiology of tension headache
A
- Muscle contraction is either normal or slightly increased and the extent of muscle contraction does not correlate with the extent of head pain.
- Psychological stress is the most common trigger for tension-type headache.
- Extended periods of mental tension or psychological stress may play a role in central sensitisation and the development of chronic tension-type headache.
- Disturbed sleep patterns can trigger an episodic tension-type headache
22
Q
Describe epidemiology of tension headache
A
- 42% mean global prevalence
- Most common onset age 20-30
- More common in females (2:3 male to female ratio)
23
Q
Describe prognosis of tension headache
A
- Infrequent episodic tension-type headache is self-limiting and simple analgesia is usually effective.
- Chronic TTH can evolve from frequent episodic TTH, with daily or very frequent episodes of headache. It is a serious condition which decreases quality of life and leads to high disability.
24
Q
List headache red flags
A
- Sudden onset, severe thunderclap headache (subarachnoid haemorrhage)
- New onset over 50 years
- Significant change in characteristic
- Fever, rash, photophobia, neck stiffness (meningism)
- Visual disturbance
- Vomiting
- Recent head trauma
- Triggered by valsalva (eg. cough) or changes in posture
- Neurological deficit
- History of malignancy or immunosuppression
- Symptoms suggestive of GCA
25
Q
List signs and symptoms of spinal cord compression/cauda equina
A
- Bilateral sciatica
- Leg weakness
- LMN at level of the lesion, UMN below the lesion (eg. Hyperreflexia, hypertonic) - not cauda equina
- Urinary hesitance or incontinence
- Faecal incontinence
- Sensory disturbance including saddle anaesthesia
- Reduced anal tone
26
Q
List signs and symptoms of spinal fracture
A
- Sudden onset, central spinal pain
- Relieved on lying down
- History of trauma
- Risk factors including steroid use
27
Q
List signs and symptoms of malignancy in the spine
A
- Age over 50
- Gradual onset
- Night pain
- Localised spinal tenderness
- Unexplained weight loss
- History of cancer
28
Q
List signs and symptoms of infection in the spine
A
- Fever
- History of infection (TB, recent UTI)
- Diabetes
- IV drug use
- HIV infection
- Immunosuppressive therapy
29
Q
Compare cauda equina and spinal cord compression
A
Cauda equina
- Flaccid paralysis asymmetrical
- Decreased or absent reflexes
- Saddle anaesthesia which is asymmetrical
- Faecal incontinence/urinary retention
Spinal cord compression (UMN)
- Spastic paralysis, symmetrical
- Increased reflexes
- Specific anatomical level of sensory defect which si symmetrical
- Faecal/urinary incontinence
30
Q
List causes of tremor
A
- Physiological
- Essential (hereditary)
- Parkinsons
- Intention
31
Q
Describe physiological tremor
A
- Fine, fast postural tremor
- Similar to hyperthyroidism, alcohol/caffeine excess, side effect of beta agonist bronchodilators
32
Q
Describe essential tremor
A
- Postural, worse when arms are outstretched
- Improved by alcohol and rest, worsened by stress, caffeine and sleep deprivation
- Titubation (head nodding)
- Family history (autosomal dominant)
- Presents over age 40
33
Q
Describe parkinsons tremor
A
- Slow, coarse, pill rolling
- Worse at rest
- Reduced with voluntary movement
- Upper limbs more affected
- Asymmetrical
- Doesn’t affect head
34
Q
Describe intention tremor
A
- Absent at rest
- Maximal on movement and approaching target
- Cerebellar pathology
35
Q
Define bells palsy
A
An acute, unilateral facial nerve weakness or paralysis of rapid onset (less than 72 hours) and unknown cause.
36
Q
Describe aetiology of bells palsy
A
Herpes simplex virus, varicella zoster virus, and autoimmunity may contribute to the development of Bell’s palsy, but the significance of these factors remains unclear.
37
Q
Describe epidemiology of bells palsy
A
- Affects 20–30 people per 100,000 each year.
- It most common between 15 and 45 years of age.
38
Q
List possible complications of bells palsy
A
- Eye injury
- Face pain
- Dry mouth
- Intolerance to loud noises
- Abnormal facial muscle contraction during voluntary movements
- Psychological sequelae
39
Q
List symptoms of bells palsy
A
- Rapid onset (less than 72 hours).
- Facial muscle weakness (almost always unilateral) involving the upper and lower parts of the face. This causes a reduction in movement on the affected side, often with drooping of the eyebrow and corner of the mouth and loss of the nasolabial fold.
- Ear and postauricular region pain on the affected side.
- Difficulty chewing, dry mouth, and changes in taste.
- Incomplete eye closure, dry eye, eye pain, or excessive tearing.
- Numbness or tingling of the cheek and/or mouth.
- Speech articulation problems, drooling.
- Hyperacusis.
40
Q
Describe diagnosis of bells palsy
A
Made when no other medical condition is found to be causing facial weakness or paralysis
41
Q
Describe management of bells palsy
A
- Keep the affected eye lubricated by using lubricating eye drops during the day and ointment at night. The eye should be taped closed at bedtime using microporous tape, if the ability to close the eye at night is impaired.
- For people presenting within 72 hours of the onset of symptoms, prescription of prednisolone should be considered.
- Antiviral treatment alone is not recommended, but it may have a small benefit in combination with a corticosteroid; specialist advice is recommended if this is being considered.
42
Q
Define horners syndrome
A
A neurological disorder characterized by a symptom triad of miosis, partial ptosis), and facial anhidrosis.
43
Q
Define cluster headache
A
Cluster headache is a rare but severe headache disorder which may be:
- Episodic cluster headache — attacks occur in periods lasting from 7 days to 1 year and are separated by pain-free periods lasting at least 1 month.
- Chronic cluster headache — attacks occur for more than 1 year without remission, or with remission periods lasting less than 1 month.
- Often occur at the same time of day, waking the person from sleep
Most common trigeminal autonomic cephalalgia
44
Q
Describe aetiology and risk factors for cluster headache
A
- The aetiology of cluster headaches is not fully understood — acute attacks involve activation in the region of the posterior hypothalamic grey matter.
- Acute cluster headache may be inherited as an autosomal dominant condition in about 5% of people.
- Factors such as previous head trauma, cigarette smoking and alcohol intake have been associated but no causal relationship identified.
- There may be an interaction between genetic and environmental factors.
45
Q
Describe the epidemiology of cluster headaches
A
- Estimated one-year prevalence of 53 per 100,000 adults and a lifetime prevalence of 124 per 100,000.
- The typical age of onset of cluster headache is 20 to 40 years.
- 70% of patients report onset before 30 years of age.
- Males are affected about four times more than females overall.
- The male-to-female ratio is markedly higher for chronic cluster headache (15:1) than for episodic cluster headache (3.8:1).
- Most people (80-90%) have episodic cluster headache with recurrent bouts separated by remission periods of more than a month.
46
Q
List symptoms of cluster headaches
A
- Unilateral periorbital pain.
- Ipsilateral autonomic symptoms such as conjunctival injection and/or lacrimation, nasal congestion and/or rhinorrhoea, eyelid oedema, forehead and facial sweating or flushing.
- Pain may be described as pulsating, boring, burning, or pressure-like.
- Attacks last between 15 and 180 minutes.
- Trigger for attacks (eg. alcohol, histamine, physical exertion, sleep or the smell of volatile substances such as perfume or petrol)
47
Q
List signs of cluster headaches
A
During an attack the person is characteristically restless or agitated, cannot lie still and may pace the floor.
48
Q
Describe investigations of cluster headaches
A
Clinical diagnosis
- At least five attacks of severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15–180 minutes and
- Headache associated with at least one of: ipsilateral conjunctival injection and/or lacrimation; nasal congestion and/or rhinorrhoea; eyelid oedema; forehead and facial sweating or flushing; a sensation of fullness in the ear; or miosis and/or ptosis; and/or a sense of restlessness or agitation.
- Attacks occur between one every other day and eight per day for more than half of the time when the disorder is active.
- The headache is not better accounted for by another ICHD-3 diagnosis.
49
Q
Define Guillian Barre syndrome
A
- Guillain-Barre syndrome is an acute inflammatory demyelinating polyneuropathy (AIDP).
- It typically comes on several weeks after viral infection, usually, GI or URTI . HIV is also known to be a cause.
50
Q
Describe epidemiology of Guillian Barre syndrome
A
- 1-2 per 100 000/ 1 in 50000 per annum
- In 40% of cases, no cause is found
51
Q
Describe aetiology and risk factors for Guillian Barre
A
- It typically comes on several weeks after viral infection, usually, GI or URTI (also sometimes flu vaccine [controversial]). Causal pathogens include campylobacter jejune, CMV and HIV
- HIV is also known to be a cause.
- The viral infection causes the production of auto-immune antibodies against peripheral nerves. Myelin is damaged, and transmission is reduced or even blocked.
52
Q
List symptoms of Guillian Barre syndrome
A
- Symmetrical muscle weakness, that usually begins in the lower legs, and ascends to the upper limbs, and even the face.
- Usually it progresses over about 4 weeks before recovery
- It may advance very quickly, affecting all limbs at once, and resulting in paralysis
- Pain is common
- Difficulty swallowing, breathing, moving
- Miller Fischer syndrome optjalmoplegia, areflexia and ataxia with no muscle weakness
53
Q
List signs on examination of Guillian Barre syndrome
A
- Trunk, respiratory and cranial nerves can also be affected – again helping differentiate from other neuropathies.
- Autonomic signs – sweating, tachycardia, dysrythmias, respiratory involvement
- Sensory signs often absent, reflexes absent or reduced
- Reduced power, problems with balance and coordination
54
Q
List investigations performed for Guillian Barre syndrome and their results
A
- Lumbar puncture – increased protein in the CSF, white cell count normal (albuminocytologic dissociation)
- Nerve conduction studies/ EMG – slowed. MRI spine.
- FVC to monitor lung function - if less than 2 call ITU
- Bloods (anti-ganglioside antibodies in Miller Fischer and 25% GB)
55
Q
Define myasthenia gravis
A
Myasthenia Gravis is an acquired, autoimmune disease of the neuromuscular junction due to antibodies produced against nicotininc acetylcholine receptor(fatigability)
56
Q
Describe aetiology and risk factors of myasthenia gravis
A
- Antibodies attack the Acetylcholine receptor.
- Therefore, the nerve signal is not fully transmitted, and the resultant muscle weakness is a result of incomplete stimulation, rather than an inherent disorder within the muscle.
- Strong association with disorders of thymus, with 75% patients having thymus hyperplasia/atrophy
- Personal or family history of autoimmune diseases.
- Under 50 commoner in females, over 50 commoner in males
57
Q
Describe epidemiology of myasthenia gravis
A
- The prevalence of Myasthenia Gravis is about 1 in 5,000.
- Although anyone is susceptible to it, there are two main subgroups, young women (20-35) and older men (60-75).
58
Q
List symptoms and signs of myasthenia gravis
A
- Ocular- Diplopia and ptosis
- Bulbar-Dysphagia, Dysphonia, Dysarthria and weak/droopy face
- Proximal muscle weakness- Shoulders and Thighs
- Axial weakness – Neck and trunk, but also muscles involved in Respiration
- Generally periods of remission and crises
- Weakness is worse with use (therefore, worst at the end of the day)
- Limb reflexes are usually normal or brisk, and there are no sensory abnormalities.
- Muscle wasting is usually not present, unless there is severe disease, or the patient has had the condition for a long time.
- Fatiguability
59
Q
Describe investigations for myasthenia gravis and their results
A
- TENSILON test, in which patients are given two drugs, Edrophionium, which prevents breakdown of acetylcholine, and atropine to prevent cardiac side effects associated with Edrophionium. If the patient has myasthenia gravis, then within seconds there is a dramatic symptomatic improvement, however this goes after a couple of minutes.
- Blood tests for serum acetylcholine receptor antibodies are positive in over 85% of patients with Myasthenia gravis, and there may also be other autoantibodies present, usually against muscle, joints or the thyroid.
- Electromyography is used to measure how fatigable a muscle is. Electricity is used to repeatedly stimulate a muscle, fatigue can be seen. Single fibre electromyography is usually preferred, as stimulating a single motor unit (remember those, a motor neurone and the muscle fibres it supplies), a variability called a ‘jitter’ can be found.
- CT/ MRI scans are used to image the thymus, looking in particular for hyperplasia and thymoma
- Spirometry is important as it gives an indication as to how badly affected the respiratory muscles are. In some crises respiratory function is compromised, and urgent medical attention is needed.
- Ptosis improves after ice compression
60
Q
Compare central facial nerve palsy and peripheral facial nerve palsy
A
- Central facial nerve palsy causes weakness or paralysis of the contralateral face that spares the muscles of the forehead, due to bilateral upper motor neuron innervation of the upper face.
- Peripheral facial nerve palsy affects all muscles of facial expression on the ipsilateral side.
61
Q
Define parkinsons disease
A
Parkinson’s disease is a chronic, progressive neurodegenerative condition resulting from the loss of the dopamine-containing cells of the substantia nigra.
62
Q
Define parkinsonism
A
- Parkinsonism is an umbrella term for the clinical syndrome involving bradykinesia together with at least one of the following: rigidity, tremor, and postural instability.
- Parkinson’s disease is the most common form of parkinsonism.
- Other causes of parkinsonism include drug-induced, cerebrovascular disease, Lewy body dementia, multiple system atrophy, and progressive supranuclear palsy.
63
Q
Describe risk factors and aetiology of Parkinsons Disease
A
- Not fully understood
- Mainly genetic risk factors
- Loss of dopaminergic neurones in the substantia nigra associated with lewy bodies in the basal ganglia, brainstem and cortex
64
Q
Describe epidemiology of Parkinsons Disease
A
- Parkinson’s disease is a common condition in elderly people, with a prevalence of 1–2% in people older than 65 years of age.
- 3.5% in 85-89 years
65
Q
List signs and symptoms of Parkinsons disease
A
- Bradykinesia
- Hypokinesia (reduced facial expression, arm swing, or blinking, difficulty with fine movements such as buttoning clothes and opening jars, or small, cramped handwriting (micrographia), slow, shuffling, festinating gait, narrow, or difficulty turning in bed.)
- Stiffness or rigidity predominantly affecting the side of onset (lead-pipe rigidity, which describes the constant resistance felt when a limb is passively flexed in the presence of increased tone without tremor, cogwheel rigidity, which describes the regular intermittent relaxation of tension felt when a limb is passively flexed in the presence of tremor and increased tone.)
- Rest tremor, which usually improves on moving, with mental concentration, and during sleep, may affect the thumb and index finger (‘pill-rolling’), the wrist, or the leg. It may also affect the lips, chin, and jaw, but rarely involves the head, neck, or voice.
- Balance problems and/or gait disorders.
- Postural instability is suggested by the ‘pull test’ — a tendency to fall backwards after a sharp pull from the examiner. This may be suggestive of Parkinson’s disease if unrelated to primary visual, cerebellar, vestibular, or proprioceptive dysfunction.
Unilateral in early disease, becomes bilateral
General symptoms:
- Depression, anxiety, and fatigue.
- Reduced sense of smell.
- Cognitive impairment.
- Sleep disturbance.
- Constipation.
66
Q
Describe investigations of Parkinsons disease
A
- History
- Signs and symptoms
- Examination
- Exclude other causes of parkinsonism (eg. drug induced, cerebrovascular, lewy body dementia…)
- Consider MRI to rule out other causes
- Dopaminergic agent trial (improvement in symptoms)
67
Q
Define multiple sclerosis
A
- Multiple sclerosis (MS) is an acquired, chronic, immune-mediated, inflammatory condition of the central nervous system (CNS) that can affect the brain, brainstem, and spinal cord.
- The inflammatory process causes areas of demyelination (damage to white matter), gliosis (scarring), and neuronal damage throughout the CNS.
- Onset usually in young adulthood
68
Q
Describe patterns of disease in multiple sclerosis
A
- Relapsing-remitting MS (most common pattern of disease — about 85% of people - exacerbations of symptoms are followed by recovery and periods of stability)
- Secondary progressive (gradual accumulation of disability unrelated to relapses, which become less frequent or stop completely, about two thirds of people with RMS progress to SPMS)
- Primary progressive MS (steady progression and worsening of the disease from the onset, without remissions occurs in about 10–15% of people with MS)
69
Q
Describe aetiology of MS
A
- Cells of the immune system, mainly T-cells, attack oligodendrocytes, resulting in focal or diffuse areas of inflammation that is thought to cause secondary damage, primarily to axons.
- Re-myelination of axons may occur in remissions, but may be partial or transient.
- Progressive damage to affected cells in the nervous system leads to irreversible loss of function of affected nerves, resulting in permanent symptoms and signs.
70
Q
List risk factors for MS
A
- Genetics (20% blood relative with MS)
- Vitamin D deficiency
- Smoking
- Diet and obesity in early life
- Latitude (prevalence increases further from euator)
- Epstein Barr virus
- Female gender (2-3 times more common in women)
- Associated with HLA-DR2
71
Q
Describe epidemiology of MS
A
- Most common non-traumatic cause of neurological disability in people under 40
- 2.3 million people worldwide in 2016
- Mean age of diagnosis is 30, most common 20-50
- RRMS affects 85% of people with MS
- 2-3 more times common in women
- More common in northern populations in UK
72
Q
List common symptoms of MS
A
- Loss or reduction of vision in one eye with painful eye movements (optic neuritis, partial or total unilateral vision loss with pain behind the eye)
- Diplopia.
- Ascending sensory disturbance and/or weakness.
- Balance problems, unsteadiness, or clumsiness.
- Altered sensation radiating down the back and sometimes into the limbs on neck flexion (Lhermitte’s symptom).
- Urinary symptoms (urgency, frequency, retention)
- Speech and swallowing difficulties
- Fatigue
- Heat intolerance
- Sexual dysfunction
73
Q
List signs of MS
A
- Optic neuritis (loss of colour discrimation, disc may appear pale or swollen. RAPD)
- Transverse myelitis (sensory and motor symptoms, focal muscle weakness reduced sensation and muscle tone initially reduced)
- Cerebellar signs (ataxia, vertigo, dysmetria)
- Brainstem signs (ataxia, oscillopsia, nystagmus, internuclear opthalmoplegia (inability to adduct one eye with nystagmus in abducting eye))
- Dysarthria and dysphagia
74
Q
Describe diagnosis of MS
A
- Diagnosed by consultant neurologist based on McDonald criteria
- FBC, inflammatory markers, liver, renal function, calcium, HbA1c, thyroid function, B12 and HIV should be tested to exclude differentials
- 2 lesions separated in time and space
- MRI showing plaques, especially in the corpus callosum. GAD enhanced shows new lesions up as brighter
- LP abnormal immunoglobulins (oligoclonal bands)
- VIsual evoke potentials are slowed
75
Q
Compare spasticity and rigidity
A
- Spasticity is where there is a lot of resistance in the muscle and it eventually gives way. This is caused by upper motor neuron lesions. It is called clasp knife rigidity
- Rigidity is sustained resistance, also called lead pipe rigidity. It is extrapyramidal. When caused by parkinsons it is called cog wheel rigidity
76
Q
Describe GCS
A
Eye 1- does not open eyes 2- opens eyes in response to pain 3-opens eyes in response to voice 4- opens eyes spontaneously
Verbal 1 - Makes no sounds 2 - Makes sounds 3 - Words 4 - Confused, disoriented 5 - Oriented, converses normally
Motor
1 - Makes no movements
2 - Extension to painful stimuli (decerebrate response)
3 - Abnormal flexion to painful stimuli (decorticate response)
4 - Withdrawal to painful stimuli
5 - Localizes to painful stimuli
6 - Obeys commands
77
Q
Describe the MRC muscle power scale
A
0 - No contraction
1 - Flicker or trace of contraction
2 - Active movement with gravity eliminated
3 - Active movement against gravity
4 - Active movement against gravity and resistance
5 - Normal power
78
Q
Describe what is looked for in general inspection in cranium exam
A
- Squint
- Ptosis
- Facial droop
- Asymmetrical or abnormal eye position and pupils
79
Q
List what is looked for in general inspection in limb exam
A
- Fasciculations
- Muscle wasting
- Scars
- Neurofibromas
80
Q
Define subdural heamatoma, and list the types
A
- A subdural haematoma (SDH) is a collection of clotting blood that forms in the subdural space.
- May be acute SDH.
- A subacute SDH (this phase begins 3-7 days after the initial injury).
- A chronic SDH (this phase begins 2-3 weeks after the initial injury).
- A simple SDH is when there is no associated parenchymal injury.
- A complicated SDH is when there is associated underlying parenchymal injury, such as contusion.
81
Q
List risk factors for subdural haematom
A
- Infants (tearing of bridging veins in the subdural space, physical abuse)
- Elderly (cerebral atrophy causing tension on veins)
- Alcohol (thrombocytopenia, blunt head trauma)
- Anticoagulation treatment
- Falls
82
Q
Describe epidemiology of subdural haematoma
A
- 1/3 people with severe head injury
- More common with increasing age 7.35 per 100000 population age 70-79
- Infants 12.5 per 100000
83
Q
Describe symptoms of subdural haematoma
A
- Gradual onset of headache
- Acute - shortly after head injury, fluctuating consciousness, patient may initially appear well
- Chronic - 2,3 weeks after trauma, symptoms are progressive, anorexia, nausea or vomiting.
- Neurological deficit (limb weakness, speech difficulties, drowsiness or confusion or personality changes)
- Headache
84
Q
Describe investigations of subdural haematoma
A
- GCS
- Vital signs
- Neuro exam
- FBC, U and Es, LFTs
- Coagulation screen
- Cross match blood
- CT scan of head (crescent of blood around outer edge of brain)
- Subacute uses contrast or MRI
85
Q
List signs of subdural haematoma
A
- Papilloedema
- Bradycardia and hypertension
- Raised intracranial pressure
- Seizures
86
Q
Describe treatment of subdural haematoma
A
- ABCDE
- If under 10mm and no significant neurological dysfunction observe + antiepileptics (levetiracetum) + lower ICP (raised head of bed, analgesics and sedation
- Over 10mm irrigation, evacuation, burr hole craniostomy (preferred if chronic)
- Craniotomy (preferred if acute), duraplasty
- Find cause of trauma
87
Q
List complications of subdural haematoma
A
- Death due to cerebellar herniation
- Cerebral oedema
- Recurrent haeatoma during recovery
- Seizures
- Wound infection, subdural empyema, meningitis
- Permanent neurological or cognitive deficit due to pressure effects
- Coma
