Neurology Flashcards
1
Q
What is a TIA?
A
- Transient ischaemic attack.
- A transient episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischaemia.
- Symptoms resolve within 24 hours, usually within 1 hour.
2
Q
What is the clinical presentation of a TIA?
A
- Sudden onset and brief duration of symptoms.
- Symptoms will represent a focal neurological deficit.
- Basically a shorter version of a stroke.
3
Q
What are the risk factors for a TIA?
A
- Atrial fibrillation.
- Mitral valve stenosis.
- Carotid stenosis.
- Congestive heart failure.
- Hypertension.
- Diabtes mellitus.
- Smoking.
- Older age.
4
Q
What is the pathophysiology of TIA?
A
- Partial blood flow restriction.
- Leads to neuronal dysfunction, but delays neuronal death (infarction) as there is still a partial supply of blood.
- If the partially occluding thrombus is autolysed quickly enough, blood flow is restored and neuronal death will be prevented.
- Causes reversal of neurological symptoms.
5
Q
What are the investigations used in a TIA?
A
TIA is a clinical diagnosis primarily.
- ROSIER (ER assessment)/ FAST (outside of hospital) used to screen/diagnose TIA.
- Blood glucose levels checked (hypoglycaemia can mimic the symtpoms of a TIA/stroke).
- Non-contrast CT head not typically used. However, will be used if the patient has a bleeding disorder/ is currently taking anticoagulants (e.g. warfarin) as they are at higher risk of haemorrhage.
- ABCD2 can be used after a TIA to calculate the risk of stroke in
6
Q
What is the ABCD2 score?
A
Assesses risk of stroke following a TIA:
A - Age>60? +1
B - BP>140/90? +1
C - Clinical features of TIA.
Speech disturbance without weakness? +1
Unilateral weakness? +2
D - Duration of symptoms.
>10 mins? +1
>60 mins? +2
^2 - History of diabetes? +1
6 or more is high risk.
7
Q
What treatment can be given for a TIA?
A
- Give a loading dose of aspirin (an antiplatelet) if TIA suspected.
- When TIA confirmed, swap aspirin to clopidogrel (P2Y12 inhibitor) and continue clopidogrel as secondary prevention from this point onwards.
- Start atorvastatin immediately (and continue as secondary prevention).
8
Q
What is a stroke?
A
- Rapid onset of either focal or global neurological deficit with no apparent cause other than that of vascular origin.
- Symptoms last MORE THAN 24 HOURS (unlike a TIA).
9
Q
What are the two types of stroke?
A
- Ischaemic (Caused by vascular occlusion/stenosis leading to ischaemia of the brain).
- Haemorrhagic (vascular rupture causes subarachnoid or intraparenchymal haemorrhage.
10
Q
What are the risk factors for stroke?
A
- Old age.
- FH of stroke.
- Previous stroke/TIA.
- Diabetes mellitus.
- Smoking.
- High BP.
- Atrial fibrillation (AF).
11
Q
What is the general clinical presentation of a stroke?
A
- Unilateral weakness in face, arm, leg.
- Unilateral sensory loss.
- Extremely painful headache.
- Speech impairments (dysarthria, dysphasia etc.)
- Loss of coordination/change of gait.
- Vertigo/loss of balance.
12
Q
What is the pathophysiology of an ischaemic stroke?
A
- Stroke is caused by either a permanent or transient occlusion of blood flow due to arterial occlusion or stenosis. There are three main mechanisms for this:
- Primary vascular pathology (e.g. vasculitis, atherosclerosis).
- Cardiac pathology (E.g. AF, patent foreamen ovale).
- Haematological pathology (e.g. sickle cell anaemia, hypercoagulapathies).
13
Q
What is the pathophysiology of a haemorrhagic stroke?
A
- Vascular rupture with bleeding into the brain parenchyma, causing primary mechanical brain damage.
14
Q
What are the two tools used to initially recognise/diagnose stroke in the community and in a hospital?
A
- FAST (Face, arms, speech test) is used in the community to screen for a potential stroke.
- ROSIER (Recognition of stroke in emergency room) is used in the ER to quickly diagnose stroke.
15
Q
What is the initial management of a suspected stroke?
A
- Admit to specialist acute stroke unit.
- GCS (Glasgow coma score).
- Measure blood glucose (to exclude hypoglycaemia, which can mirror the presentation of stroke).
- Refer for urgent non-contrast CT head scan. This will determine if the stroke is haemorrhagic or ischaemic.
16
Q
What is the management following confirmation a stroke is ischaemic?
A
- IF WITHIN 4.5 HOURS OF SYMPTOM ONSET give altepase (a thrombolytic drug).
- Aspirin ASAP (or clopidogrel if aspirin not tolerated).
- Thrombectomy if there is potential to save some of the brain tissue.
- After 48 hours, start high dose atorvastatin.
- ANTCOAGULANTS (WARFARIN, HEPARIN) ARE NOT INDICATED.
17
Q
What is the treatment following confirmation a stroke is haemorrhagic?
A
- Supportive treatment (O2, fluids, BP monitoring, ICP monitoring etc.)
NOTE: Only give O2 if <94% - Urgent reversal of anticoagulants (warfarin is reversed using vit K/prothrombin complex concentrate.
- Immediate referral to neurosurgery.
- DO NOT START A STATIN.
18
Q
What are the key symptoms suggestive of disrupted blood supply in each of the cerebral arteries?
A
- Anterior cerebral artery (ACA) will generally present with contralateral leg weakness.
- Medial cerebral artery (MCA) will generally with contralateral face/arm weakness.
- Posterior cerebral artery (PCA) will generally present with homonymous hemianopia and memory loss (hippocampus supplied by the PCA).
19
Q
What is a subarachnoid haemorrhage?
How does it present on a CT scan?
A
- Spontaneous arterial bleeding into the subarachnoid space, between the pia and the arachnoid layers.
- Presents as a star pattern on a CT scan.
20
Q
What is a subdural haemorrhage?
How does it present on a CT scan?
A
- Bleeding occurring between the dura and arachnoid layers.
- Presents as a crescent on a CT scan.
21
Q
What is a extradural haemorrhage?
How does it present on a CT scan?
A
- Bleeding occurring in the potential space between the skull and the dura.
- Presents as a convex lens (otherwise known as lentiform) shape.
22
Q
What are the four categories of stroke within the Bamford classification?
A
- Total anterior circulation stroke (TACS).
- Partial anterior circulation stroke (PACS).
- Posterior circulation syndrome (POCS).
- Lancunar Stroke (LACS
23
Q
How is the Bamford classification used?
A
Anterior stroke criteria. Total anterior circulation stroke (TACS) needs 3/3, partial anterior circulation stroke (PACS) needs 2/3:
- Unilateral loss of motor and/or sensory function in face, arm and leg.
- Homonymous hemianopia.
- Higher cerebral disfunction (e.g. speech difficulty).
Posterior circulation syndrome criteria. POCS must meet 1 of the following criteria:
- ISOLATED homonymous hemianopia.
- Bilateral motor/sensory deficit.
- Cranial nerve palsy that is contralateral to the motor/sensory deficit.
- Cerebellar dysfunction (nystagmus, ataxia etc.)
- Conjugate gaze palsy (Inability to move both eyes in the same direction).
Lancunar stroke criteria. LACS must meet one of the following criteria:
- Purely motor and/or sensory stroke with NO LOSS OF HIGHER CEREBELLAR FUNCTIONS.
- Ataxia hemiparesis. (This is ataxia on one side of the body).
24
Q
What is higher cerebral function?
A
Refers to conscious mental activities. For example:
- Thinking.
- Remembering.
- Reasoning.
25
Which type of heamorrhage causes thunderclap headache?
- Subarachnoid haemorrhage.
26
What are the typical causes of each type of haemorrhage?
Extradural haemorrhage - Middle meningeal artery rupture due to temporal bone break.
Subdural haemorrhage - Due to bridging vein rupture (e.g. shaken baby, old, alcoholics).
Subarachnoid haemorrhage - Caused by rupture of berry aneurysms.
27
Which type of haemorrhage is associated with CN III palsy?
- Extradural haemorrhage.
28
Which type of haemorrhage is associated with Marfan's syndrome?
Briefly, what is Marfan's syndrome and how does it relate to brain haemorrhage?
- Subarachnoid haemorrhage.
- Marfan's syndrome. An inherited condition that affects the connective tissues of the body. This weakens the blood vessel walls, making them susceptible to aneurysm.
29
What is a lucid interval and which type of cerebral haemorrhage is it associated with?
- Extradural haemorrhage.
- Patient initially is knocked unconscious.
- Then, brain compensates and the patient will appear to briefly recover. This is the "lucid recovery".
- Then, as the haemorrhage expands and ICP builds, the patient will again be knocked unconscious.
30
What is the relationship between brain haemorrhage and haemorrhagic stroke?
Haemorrhage CAN cause haemorrhagic stroke, but not all haemorrhages are strokes.
Treatment for a haemorrhage refers to a haemorrhage alone, rather than a haemorrhagic stroke.
31
What is the management for a subarachnoid haemorrhage (non-stroke)?
- Monitor GCS.
- ABC
- Nimodipine (A CCB). Used to reduce risk of late-onset cerebral ischaemia.
- Reverse anticoagulation/antiplatelets (e.g. warfarin reversal with vit K).
- Paracetamol for analgesia (AVOID NSAIDS, can affect the clotting cascade).
32
What is the management of a subdural haemorrhage?
- Continue to assess GCS.
- ABC.
- Phenytoin (an anti-convulsant) should be given prophylactically to prevent seizure.
- Reversal of anticoagulation/antiplatelets (e.g. reverse warfarin with "Prothrombin Complex Concentrate" - this is vit. K).
- Raise bed to 30 degrees to lower ICP. 2nd line is mannitol.
33
What is epilepsy?
- Umbrella term for a condition where there is a tendancy to have seixures.
34
What are the 5 main types of seizures seen in epilepsy and what do they present like?
Tonic-clonic - Period of stiffness followed by period of jerking. Most common type of seizure.
Focal - Occurs in the temporal lobe. Affects emotions, memory, speech and hearing (Deja vu, hallucinations, memory flashbacks, strange actions).
Absence - Loses awareness of surrounding and becomes unresponsive for a short period of time. Most common in children and usually resolves as they get older.
Myoclonic - Period of muscles tensing, stiffness.
Atonic - Muscles relax and person goes "floppy".
35
What is status elepticus?
Management?
- A seizure that lasts over 5 minutes
OR
- More than one seizure in the space of 5 mins, where consciousness is regained briefly between the seizures.
- THIS IS CONSIDERED A MEDICAL EMERGENCY.
Management:
0-5 mins:
- ABC (especially high flow oxygen, secure airway).
- Monitor GCS.
- Glucose + B1 (thiamine - to prevent Wernicke's encephalopathy).
- Manage acidosis.
5-20 mins:
- Lorazepam (benzodiazepam)
- Dose of 1st line anticonvulsant (normally sodium valproate - a GABA receptor agonist).
- Consider CT head if there is focal pathology/patient has no seizure history.
20-40 mins:
- 2nd line anticonvulsant (usually carbamazepine/lamotrigine - a sodium channel blocker).
- Notify ICU.
- Potentially LP if CNS infection suspected.
40 mins+:
- Transfer to ICU.
36
What is the treatment for epilepsy?
FOR ALL TYPES EXCEPT FOCAL:
- Sodium valproate is 1st line (GABA receptor agonist).
- Carbamazepine/lamotrigine is 2nd line (Sodium channel blocker).
FOR FOCAL:
- Carbamazepine/lamotrigine is 1st line.
- Sodium valporate is 2nd line.
FOR MID-SEIZURE CONTROL:
- Lorazepam (1st line) or diazepam (2nd line) (benzodiazepam)
37
What are some of the most common epileptic triggers?
3 most common are:
- Alcohol.
- Lack of sleep.
- Poor adherance to treatment.
Other causes are:
- Flashing lights
38
What are the diagnostic tests used for epilepsy?
- EEG (+ video is GS).
- MRI brain (check for structural abnormality and cancers).
- ECG (check for cardiac abnormalities, potentially causing syncope).
39
What are the risk factors for epilepsy?
- Family history.
- Trauma affecting the brain.
- Previous CNS infection.
40
What is Parkinson's disease?
The neurodegenerative loss of dopamine-secreting cells from the substantia nigra.
41
What is the clinical presentation of Parkinson's disease?
- Rest tremor
- Rigidity and bradykinesia, developed over several months
- Characteristic stoop.
- Pill rolling tremor
Remember "TRAP":
- Tremor
- Rigidity
- Akinesia
- Postural instability (tendency to fall).
42
What is the pathophysiology of Parkinson's disease?
- Progressive loss of dopamine secreting cells from the substantia nigra.
- Leads to alteration in the neural circuits that control movement/coordination.
43
What is the substantia nigra?
A basal ganglia structure, responsible for movement and coordination.
44
What is the aetiology of Parkinson's disease?
- Unknown
- Some genetic link
- Some environmental link.
45
What is the epidemiology of Parkinson's disease?
- Less common in smokers!
46
What are the diagnostic tests for Parkinson's disease?
1st line:
- Clinical diagnosis, followed by trial of a dopaminergic agent to see if there is an improvement.
2nd line:
- MRI or CT scan to assess any atrophy of the substantia nigra.
47
What are the treatment options for Parkinson's disease?
1st line:
- carbidopa (decarboxylase inhibitor) AND levidopa (CNS agent) in the same pill. Often called L-DOPA.
2nd line:
- Ropinirole (dopamine agonist).
48
What is migraine?
- Recurrent headache for 4-72 hours with visual and/or GI disturbance.
49
What are the 3 main subtypes of migraine and what makes each one different?
- Aura. Unilateral migraine with visual disturbance. Can also make person photosensitive and nauseated.
- Without aura. Unilateral migraine WITHOUT visual disturbance. Can also make the person photosensitive and nauseated.
- Variant. Unilateral migraine with various motor and sensory symptoms resembling a stroke.
50
What is the pathophysiology of migraine?
- Changes in brainstem blood flow, leading to the release of vasoactive neuropeptides (CGRO and substance P).
- This causes neurogenic inflammation, vasodilation and extravasation, resulting in the pain experienced during a migraine.
51
What is the aetiology of migraine?
- Genetic and environmental factors.
- Can be triggered by a variety of things, such as chocolate, cheese and too much/little sleep.
52
What is the epidemiology of migraine?
- Most common in women.
- Usually presents before 40.
53
What are the investigations used to diagnose migraine?
1st line:
- Clinical diagnosis
2nd line:
- Neuro imaging. Can be used to rule out potential lesions.
54
What are the treatment options for migraine?
- Sometimes will pass in sleep.
If moderate:
- Painkillers (Paracetamol/NSAIDs)
If severe:
- Serotonin agonist (such as triptan) will suppress the inflammation causing the migraine.
- Ensure patient stays hydrated and consider anti-emetics if they are feeling nauseas.
55
What is multiple sclerosis?
- Autoimmune demyelination of the CNS.
56
What are the different types of MS and what are their characteristics?
- Benign. Disease relapse/remits but the general trend is neutral (not getting worse over time).
- Relapsing-remitting. Disease cycles through being better/worse, but the general trend is to get worse over time.
- Primary progressive. Disease is steadily progressing over time, with no relapse-remitting.
- Secondary progressive. Initially had relapsing/remitting MS, but it then became progressive.
57
What is the clinical presentation of MS?
- Typically seen in young adults.
- Lhermitte's sign = Tingling down the back into limbs on flexion of the neck.
May present in three ways:
- Optic. Blurred vision, unilateral eye pain.
- Brainstem. Diplopia (double vision), vertigo, dysphagia, nystagmus (repetitive, uncontrolled eye movements).
- Spinal cord. Numbness, pins and needles, potentially spastic paresis.
58
What is the pathophysiology of MS?
- Inflammation, demyelination and axonal loss of oligodendrocytes.
Occurs in particular sites more commonly:
- Optic nerve
- Periventricular white matter
- Brainstem
- Cerebellar connections
- Cervical spinal cord.
PERIPHERAL NERVES NEVER AFFECTED.
59
What is the aetiology of MS?
- Precise mechanism is unknown.
- Appears to be as a result of an inflammatory process in the CNS mediated by CD4 T and B cells.
- Exposure to EBV in early life predisposes MS development.
60
What is the epidemiology of MS?
- More common in women
- More common in populations further from the equator.
- More common in the young.
61
What investigations are used to diagnose MS?
- MRI of CNS (brain + spinal cord)
62
What is the treatment for MS?
For an acute relapse:
- Methylprednisolone (Short course of steroids).
For relapsing-remitting MS:
- Use immunomodulators: B-interferon or immunosuppressants (e.g. rituximab).
63
What is myasthenia gravis?
- Chronic autoimmune attack against the post-synaptic Ach receptors at the neuromuscular junctions.
- Causes weakness and rapid fatigue in the skeletal muscles.
64
What is the clinical presentation of myasthenia gravis?
Weakness in skeletal muscles. Causes:
- Ptosis
- Dysphasia and dysarthria.
- Weakness/ rapid fatigue in limbs
Symptoms improve after rest.
65
What is the pathophysiology of myasthenia gravis?
- Autoantibody-mediated attack on Ach receptors at the post-synaptic membranes of the NMJs.
- This causes the blockage/ loss of Ach receptors at the junctions, impairing signal transmission to the skeletal muscles.
66
What is the aetiology of myasthenia gravis?
Strong association with thymic hyperplasia:
- 10% of people with MG have thymic hyperplasia.
- 50% of people with thymic hyperplasia have MG.
67
What is the epidemiology of myasthenia gravis?
- Women more likely to have myasthenia gravis than men.
68
What are the diagnostic tests for myasthenia gravis?
1st line:
- AchR antibody analysis.
If normal, perform MuSK antibody analysis.
69
How is myasthenia gravis treated?
1st line:
- Anti-cholinesterase (pyridostigmine).
If severe:
- Immunosuppressant drugs (such as azathioprine).
If there is a myasthenia crisis:
- Intubation/ventilation
- Plasma exchange (removes autoantibodies, reducing the autoimmune response).
70
What is myasthenia crisis?
- Worsening of myasthenic weakness, resulting in the need for intubation/ventilation due to respiratory failure.
71
What is MND?
- Motor neurone disease
- Relentless destruction of motor neurones in brain and spinal cord.
72
What are the 4 types of MND I need to know about?
Which motor neurons does each type affect?
- Amyotrophic lateral sclerosis (Most common). Affects UMN and LMN.
- Primary lateral sclerosis. Affects UMN only.
- Progressive muscular atrophy. Affects LMN only
- Progressive bulbar palsy. Affects UMN and LMN of the lower cranial nerves (CN IX - XII).
73
What is the typical clinical presentation of MND?
Varies depending on the type of MND. Generally:
UPPER LIMBS:
- Reduced dexterity
- Stiffness
- Wasting of intrinsic muscles of the hand.
LOWER LIMBS:
- Tripping
- Stumbling gait
- Foot drop
BULBAR:
- Slurred speech
- Hoarseness
- Dysphagia
OVERALL MUSCLE ATROPHY AND SPASTICITY.
74
What is the pathophysiology of MND?
- Destruction of the motor neurones.
- Leads to LMN and UMN dysfunction (depending on type of MND).
- Mixed picture of muscular paralysis/atrophy.
75
What us the aetiology of MND?
Unknown. Some variants involve genetic mutations.
76
What is the epidemiology of MND?
- Middle age
- More common in men.
77
What are the investigations used in suspected MND?
1st line:
- Clinical (fasciculations are present even in the early stages of MND).
If unsure:
- EMG (electromyography)
78
What treatments are available for MND?
1st line:
- Sodium channel blockers (e.g. Riluzole)
If struggling with muscle spasticity:
- Baclofen (a skeletal muscle relaxant).
79
What are the potential complications of MND?
- Most die within 3 years, due to respiratory failure as a result of bulbar palsy and pneumonia.
80
What is meningitis?
Infection of the meninges.
81
What are the two different pathogens that can cause meningitis?
- Viruses
- Bacteria
82
What are the symptoms of meningitis?
Bacterial meningitis:
- Headache
- Neck stiffness
- Fever
- Photophobia
- Vomiting
- Kernig's sign (inability to straighten leg when knee flexed to 90 degrees)
- Progressive drowsiness
- Purpuric, non-blanching rash
Viral meningitis:
Same as above, except:
- No rash
- More benign and self-limiting.
83
Is meningitis a notifiable disease?
Yes
84
What is the pathophysiology of meningitis?
- Infection of the meninges leads to inflammation of the tissue.
85
What is the aetiology of bacterial meningitis?
Infective agents can reach the meninges from:
- Ears
- Nasopharynx
- Cranial injury
- Bloodstream
The two most common bacterial causes of meningitis in adults are:
- Neiserria meningitis
- Streptococcus pneumoniae
86
What is the aetiology of viral meningitis?
- Herpes simplex virus.
- Enterovirus.
87
What investigations are done to diagnose meningitis?
- Lumbar puncture, and subsequent CSF culture. NOT IF RAISED ICP ON CT.
- Blood culture and meningococcal and pneumococcal probe PCR.
88
What is the treatment for bacterial meningitis?
When suspected:
- ABC
- Corticosteroids (dexamethasone)
- Empirical antibiotics (cefotaxime)
After cultures arrive back, choose more pathogen specific antibiotics.
89
What is the treatment for viral meningitis?
When suspected:
- treat with empirical antibiotics until viral cause has been confirmed (cefotaxime).
When confirmed:
- ABCs
- Analgesics (Ibuprofen/paracetamol)
If viral meningitis is recurrent:
- Consider specialist referral for antibiotics.
90
What is encephalitis?
- Inflammation of the brain parenchyma (functional tissue).
91
What are the symptoms of encephalitis?
Most common:
- Fever
- Headache
- Altered behaviour and altered mental status
Can cause:
- Hemiparesis
- Dysphagia
- Seizure/coma
92
What is the pathophysiology of encephalitis?
- Infection of the brain parenchyma, leading to inflammation.
93
What is the aetiology of encephalitis?
Often presumed viral. Common viral causes are:
- Herpes simplex virus
- Coxsackie virus
- ECHO
- Mumps
94
What investigations are used to diagnose encephalitis?
FBC:
- Elevated WCC.
```
MRI brain (gold standard), but CT if not available:
- Check for space-occupying regions.
```
Viral serology:
- LP and CSF analysis
95
What is the treatment for encephalitis?
- ABCs
- Immediate start on aciclovir as soon as viral encephalitis is suspected. This is because most of the time it is due to HSV, and aciclovir is an antiviral for herpes.
- Make antiviral therapy more specific when the exact viral cause has been established.
- If ICP elevated, give steroids and mannitol.
96
What is herpes zoster (Shingles)?
- Reactivation of the varicella zoster virus (chickenpox).
97
What are the symptoms of herpes zoster virus in each of the different phases?
Pre-eruptive:
- No skin lesions yet, but burning and itching in one dermatome.
- Usually a day or two before eruption.
Eruptive phase:
- Skin lesions appear (they are infectious until dried).
- Erythematous swollen plaques.
- RASH DOES NOT CROSS DERMATOMES.
98
What is the pathophysiology of Herpes Zoster virus (shingles)?
- After infection, the virus lies dormant in the sensory nervous system ganglia.
- Eventually flares up, virus travels down the affected nerve over 3-4 days, causing perineural and intraneural inflammation.
- Eventually, the virus reaches the skin, and the typical dermatomal rash will present.
99
What is the aetiology of shingles?
- Varicella-zoster virus reactivation (now called herpes-zoster)
- Gives rise to chickenpox in childhood, but then if reactivated in adulthood can cause shingles.
100
How is shingles investigated?
- No investigation needed.
- Diagnosed based on the stereotypical rash, present within one dermatome only.
101
What is the treatment for shingles?
- Famciclovir (antiviral) 1st line.
- Aciclovir (antiviral) 2nd line.
- Analgesia as required (NSAID/paracetamol for moderate, oxycodone opiate for severe).
102
What is a primary brain tumour?
Tumour in the brain that arose from associated tissue.
103
What is a secondary brain tumour?
Tumour in the brain that metastasised from elsewhere.
104
What are the types of primary brain tumour?
- Glioma. Originates from glial cells.
- Meningioma. Tumour that arrises from the meninges surrounding the CNS (brain + spinal cord).
- Pituitary adenoma. Benign tumour of the pituitary gland.
105
What are the symptoms of a brain tumour?
Progressive focal neurological deficit:
- Symptoms depend on location.
- Speed of deterioration is proportional to growth of tumour.
Raised ICP:
- Headaches (worse on coughing/ leaning forwards).
- Vomiting.
- Papilloedema (optic disc swelling).
May develop epilepsy
General cancer symptoms:
- Weight loss
- Malaise
- Anaemia
106
What are false localising signs?
- Signs that occur due to raised ICP or tumour presence that reflect more distant pathology.
- For example, a tumour of the temporal lobe may cause a CN III palsy.
107
What is the pathophysiology of a tumour?
- Progressive focal neurological deficit is caused directly by the tumour, and will impact the area of the brain the tumour is in.
- As the tumour grows, ICP increases and the brain will be downwardly displaced.
- This puts pressure on the brainstem, causing drowsiness. Eventually, it can even cause respiratory depression, coma and death.
- Tumours can generate pathological electrical signals, causing epilepsy.
108
What is the aetiology of a primary brain tumour?
- Derived either from the skull itself or the adjacent structures.
- 95% of primary tumours are gliomas or meningiomas.
109
What is the aetiology of a secondary brain tumour?
Metastases from: bronchi, breast, kidney, thyroid, stomach and prostate.
110
What are the investigations used when a brain tumour is suspected?
- CT and MRI scan
- Biopsy (surgery)
111
What are the therapeutic options for a brain tumour?
- Surgery (removal or biopsy)
- Radiotherapy or chemotherapy.
112
What is giant cell arteritis?
- Granulomatous arteritis.
113
What is the clinical presentation of giant cell arteritis?
- Headache
- Tender scalp
- Jaw claudication
- Superficial temporal artery may be firm, tender and pulseless.
- Weight loss
- Malaise
- Fever
- Blindness occurs in 25% if left untreated.
114
What is the pathophysiology of giant cell arteritis?
- Chronic inflammation of the medium-large arteries, particularly the aorta and its extra cranial branches.
- The blindness can occur as a result of ciliary and/or central retinal artery occlusion.
115
What are the investigations used when giant cell arteritis is suspected?
Blood tests:
- Elevated ESR/CRP
If available, conduct rapid-access ultrasonography (gold standard):
- Non-compressible halo sign indicates giant cell arteritis.
- Wall thickening, stenosis and/or occlusion also indicate potential giant cell arteritis.
116
What is the treatment for giant cell arteritis?
- Administer high dose prednisolone IMMEDIATELY, even before diagnosis confirmation.
- Specialist may consider use of methotrexate if the patient is high risk/experiencing a relapse of giant cell arteritis.
117
What areas of the brain do the anterior cerebral, middle cerebral and posterior cerebral artery supply?
Anterior cerebral:
- Medial portions of frontal lobe and superior medial parietal lobe.
- Occlusion of this artery causes contralateral lower limb weakness.
Middle cerebral:
- Supplies areas of the frontal, temporal and parietal lobes.
- Occlusion causes speech impairment, contralateral weakness and hemiparesis of the lower contralateral face (with forehead sparring).
Posterior cerebral:
- Supplies occipital lobe and the hippocampus.
- Occlusion causes acute vision loss and memory impairment.
118
What does cerebellar stroke cause?
- Impairs balance and coordination.
119
What does brain stem stroke cause?
- Hemiparesis (inability to move on one side of the body)
- Can cause quadriplegia (Paralysis from the neck down)
120
What is a cluster headache?
- Attack of severe pain localised to the unilateral orbital, supra-orbital and/or temporal areas.
- Lasts 15 mins to 3 hours.
- Occurs between once every 2 days and 8 times a day.
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What is the clinical presentation of a cluster headache?
- Attacks occur at the same time for a period of weeks (called the cluster period).
- Most patients are restless or agitated.
- Can cause ptosis, facial swelling and sweating.
- Extremely painful headaches.
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What differentiates a cluster headache from a migraine?
- Migraine patients usually report motion sensitivity so try to remain still.
- Cluster headache patients are usually restless and agitated during an attack.
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What is the pathophysiology of cluster headache?
- Hypothalamic activation, along with secondary trigeminal and autonomic activation.
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What is the aetiology of cluster headache?
Cluster period attacks can be induced by:
- Alcohol
- Volatile smells
- Warm temperatures
- Sleep
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What are the risk factors associated with cluster headache?
- Family history
- Male
- Head trauma
- Smoking
- Alcohol
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How is a cluster headache normally investigated?
- Usually just a clinical diagnosis.
- MRI may be used to eliminate secondary causes.
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What is the treatment for cluster headaches?
ONGOING MANAGEMENT:
- CCB (1st line) such as verapamil.
- Lithium (2nd line).
ACUTE ATTACK MANAGEMENT:
- Subcutaneous sumatriptan (a triptan) and high flow oxygen.
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What is a tension headache?
- Tension headache can be either episodic or chronic.
- Pain is described as a tight band around the head.
- Pain does not worsen with physical activity.
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What is the clinical presentation of a tension headache?
- Dull, non-pulsatile, bilateral, constricting pain (not severe).
- Pain is typically seen in the frontal or occipital areas, but can be anywhere.
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Why are tension headaches rarely seen in clinic?
- They are usually self-managed, and very rarely disabling.
- Therefore, patients do no usually seek medical care.
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What are the common triggers of a tension headache?
- Stress
- Mental tension
- Missing meals
- Fatigue
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What investigations are typically performed for tension headache?
Clinical diagnosis:
- Look for a headache without nausea and vomiting.
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What is the treatment for a tension headache?
Simple analgesics for an acute attack (aspirin/paracetamol/ibuprofen).
For chronic headache (\>7 days per month), consider using low dose antidepressants such as amitriptyline (tricyclic antidepressant).
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What are the symptoms of:
1) A temporal seizure?
2) A frontal lobe seizure?
3) A parietal lobe seizure?
4) A occipital lobe seizure?
1) Temporal = Head
- Hallucinations
- Epigastric rising (stomach sensation).
- Emotional
- Automatisms (e.g. lip smacking)
- Deja Vu
2) Frontal lobe = motor
- Head/leg movements
- Posturing
- Post-ictal (period after seizure) weakness
3) Parietal lobe = sensory
- Parasthesia (burning/prickling sensation).
4) Occipital lobe = visual
- Eye floaters
- Flashes
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What does CN III innervate?
What eye syndrome occurs if there is a lesion in CN III?
- All eye muscles except for lateral rectus (CN XI) and superior oblique (CN IV).
- Causes "down and out" eye syndrome if lesion.
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What is CN IV called and what does it innervate?
What does a lesion of CN IV cause?
- Trochlear nerve
- Innervates Superior oblique muscle.
- Causes double vision on looking down, and upwards/outwards rotation of the affected eye.
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What is the name of CN VI and what does it innervate?
What does a lesion of CN VI cause?
- Abducens nerve
- Innervates lateral rectus muscle.
- Eye cannot be abducted, leading to it pointing inwards.
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What is the name of CN V and what does it innervate?
- Trigeminal nerve.
Sensory:
- Face, sinuses and teeth.
Motor:
- Muscles of mastication.
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What is the name of CN VII and what does it innervate?
- Facial nerve.
Sensory:
- Anterior 2/3 of tongue, and soft (posterior) palette.
Motor:
- Facial muscles (facial expression).
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What is the name of CN VIII and what does it innervate?
- Vestibulocochlear nerve.
Sensory:
- Carries information from hearing and equilibrium (balance).
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What is CN IX called and what does it innervate?
- Glossopharyngeal nerve
Sensory:
- Posterior 1/3 of tongue. (GAG REFLEX)
- Pharynx.
- Epiglottis.
Motor:
- Stylopharyngeus
- Pharyngeal constrictors
- Parotid gland
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Which is the only cranial nerve to innervate contralateral structures?
- CN IV (Trochlear nerve)
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What does CN X damage. cause?
- Soft palette droop. (uvula will therefore deviate towards the normal side.
- Gag reflex loss.
- Hoarse/nasal voice.
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What is CN XI and what does it innervate?
- Accessory nerve.
Motor:
- Laryngeal muscles, trapezius (damage makes shrugging shoulders hard).
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What is CN XII and what does it innervate?
- Hypoglossal nerve
Motor:
- Intrinsic and extrinsic tongue muscles. (damage causes tongue paralysis and eventually atrophy).
