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Phase 2 v2 > Neurology > Flashcards

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.
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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.
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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.
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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.
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5
Q

What are the scoring systems/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 to calculate stroke risk following a TIA.
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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.

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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).
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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).
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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.
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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).
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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.
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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).
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13
Q

What is the pathophysiology of a haemorrhagic stroke?

A
  • Vascular rupture with bleeding into the brain parenchyma, causing primary mechanical brain damage.
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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.
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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.
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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.
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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.
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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).
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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.
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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.
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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.
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22
Q

Which type of heamorrhage causes thunderclap headache?

A
  • Subarachnoid haemorrhage.
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23
Q

What are the typical causes of each type of haemorrhage?

A

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.

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24
Q

Which type of haemorrhage is associated with CN III palsy?

A
  • Extradural haemorrhage.
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25
Q

Which type of haemorrhage is associated with Marfan’s syndrome?

Briefly, what is Marfan’s syndrome and how does it relate to brain haemorrhage?

A
  • 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.
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26
Q

What is a lucid interval and which type of cerebral haemorrhage is it associated with?

A
  • 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.
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27
Q

What is epilepsy?

A
  • Umbrella term for a condition where there is a tendancy to have seixures.
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28
Q

What are the 5 main types of seizures seen in epilepsy and what do they present like?

A

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”.

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29
Q

What is status epilepticus?

Management?

A
  • 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:

  • ABC (especially high flow oxygen, secure airway).
  • Monitor GCS.
  • Lorazepam (benzodiazepam)
  • Dose of 1st line anticonvulsant (normally sodium valproate - a GABA receptor agonist).
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30
Q

What is the treatment for epilepsy?

A

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)
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31
Q

What are some of the most common epileptic triggers?

A

3 most common are:

  • Alcohol.
  • Lack of sleep.
  • Poor adherance to treatment.

Other causes are:

  • Flashing lights
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32
Q

What are the diagnostic tests used for epilepsy?

A
  • EEG (+ video is GS).
  • MRI brain (check for structural abnormality and cancers).
  • ECG (check for cardiac abnormalities, potentially causing syncope).
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33
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)
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34
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, memory loss, reasoning).

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).
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35
Q

What is higher cerebral function?

A

Refers to conscious mental activities. For example:

  • Thinking.
  • Remembering.
  • Reasoning.
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36
Q

What is the relationship between brain haemorrhage and haemorrhagic stroke?

A

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.

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37
Q

What is the management for a subarachnoid haemorrhage (non-stroke)?

A
  • 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).
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38
Q

What is the management of a subdural haemorrhage?

A
  • 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.
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39
Q

What is huntington’s disease, including details of the genetic cause?

A
  • Autosomal dominant neurodegenerative disorder, caused by CAG repeats.
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40
Q

What is the presentation of Huntington’s disease?

A
  • Usually presents in middle-ages (slow progression).

- +ve family history is key.

  • Chorea (involuntary, jerky movements).
  • Cognitive impairment (concentration deficit, misjudgements etc.)
  • Behaivoural changes (irritable, impulsive etc.)
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41
Q

What is the diagnostic investigation used for Huntington’s disease?

A
  • CAG repeat testing.
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42
Q

What is the treatment for Huntington’s disease?

A
  • Limited options.
  • SSRI (e.g. fluoxitine).
  • Antipsychotics.
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43
Q

What is Guillian-Barre Syndrome?

A
  • An acute inflammatory neuropathy associated with progressive symmetrical muscle weakness.
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44
Q

What is the pattern of muscle weakness observed in Guillian-Barre syndrome?

A
  • Starts in lower limbs and progressess to upper limbs.
  • Starts in the proximal muscles and extends distally.
45
Q

What is the clinical presentation of Guillian-Barre syndrome?

A
  • Usually proceeded by a GI or respiratory infection.
  • Progressive, symmetrical muscle weakness.
  • Areflexia.
46
Q

What is the mainstay treatment for Guillian-Barre syndrome?

A
  • Plasmapharesis (plasma exchange).
47
Q

What is carpal tunnel syndrome?

A
  • Signs/symptoms caused by median nerve compression in the carpal tunnel.
48
Q

What are the carpal tunnel risk factors?

A
  • Female between 40 and 60.
  • Repetative hand/wirst movements.
49
Q

What is the presentation of carpal tunnel syndrome?

A
  • Numbness/tingling in thumb/radial fingers.
  • Wrist aching.
  • Relief achieved by “flicking” the wrist.
  • Atrophy of base of thumb.
50
Q

What is the investigation used in carpal tunnel syndrome?

A
  • Electromyography (EMG).
51
Q

What is the treatment for carpal tunnel syndrome?

A
  • Wrist splint.
  • Injected corticosteroids (prednsiolone).
  • Potentially surgery if severe.
52
Q

What is MS?

A
  • Chronic inflammatory disorder of the CNS characterised by episodic neurological dysfunction that occurs at least twice disseminated in time and space.
53
Q

What is the basic pathophysiology of MS?

A
  • Demyelination of axons and loss of oligodendrocytes (Cells responsible for CNS myelination).
  • This affects signal transmission in the CNS, causing the MS symtpoms.
  • Re-myelination occurs, resulting in resolution of symptoms. Over time, this re-myelination may beome incomplete, leading to some permanent symptoms.
  • Demyelination is “disseminated in time and space”.
54
Q

What is the clinical presentation of MS?

What is Lhermitte’s sign?

A

Transient neurological symptoms that are disseminated in time and space. Symptoms commonly include:

  • Optic neuralgia. Loss of sight in one eye due to demyelination of the optic nerve.
  • Double vision. Due to demyelination of the abducens nerve (CN VI).
  • Lhermitte’s sign. (Electrical shock-like senstation down the spine and radaiting to the limbs).
  • Motor and sensory dysfunction: Demyelination of the spinal cord.
55
Q

What is the diagnostic test used for MS?

A
  • MRI spine and brain.
56
Q

What are the four types of MS and how are they differentiated? Which is the most common?

A
  • Relapsing remitting MS (MOST COMMON). This involves clear relapses with either complete or partial recovery between episodes.
  • Primary progressive MS. Continually progressing MS symptoms FROM ONSET.
  • Secondary progressive MS. Initially relapsing/remitting MS that becomes progressive.
  • Progressive/relapsing MS. Continually progressing MS symptoms with episodes of relapse/remission interspersed throughout (a combination of relapse/remitting + primary progressive).
57
Q

What is the treatment given for an acute flare of MS?

What is the treatment given for ongoing management of MS?

A

Acute flare - IV prednisolone.

Ongoing management - Interferon-beta.

58
Q

What are the risk factors for MS?

A
  • Female between 20 and 40 YO.
  • Family history.
59
Q

What is MND?

A
  • An umbrella term for disease involving motor neuron dysfunction.
60
Q

What are the key types of MND?

Which is the most common?

A
  • Amyloid lateral sclerosis. Both UMN and LMN affected.
  • Primary lateral sclerosis. Only UMN involved.
  • Progressive muscular atrophy. Only LMN involved.
  • Progressive bulbar palsy. Affects the muscles of talking and swallowing.
61
Q

What are are the symptoms of UMN disease vs LMN disease?

A

UMN - “everything goes up”

  • Increased muscle tone.
  • Increased muscle spasticity (stiffness).
  • Brisk reflexes.

LMN - “everything goes down”

  • Decreased muscle tone.
  • Atrophy.
  • Reduced reflexes.
  • Fasiculations (muscle twitching).
62
Q

What test is used in the assessment of UMN disease?

A

Babinski reflex:

  • Stimulation of sole of foot.
  • Big toe dorsiflexes and other toes fan outwards.

A normal response would be plantiflexion of the toes towards the source of the stimulus.

A positive Babinski reflex is indicative of UMN disease.

63
Q

What is the management of MND?

A
  • Riluzole (anti-oxidant).
  • Non-invasive ventilation when respiratory muscles begin to fail.
64
Q

What is the most common cause of death in MND?

A
  • Type 2 respiratory failure due to loss of respiratory muscle strength and/or endurance.
65
Q

What is meningitis?

What are the 3 typical causes?

A

Inflammation of the meninges.

Caused by:

  • Bacteria
  • Virus
  • Fungus
66
Q

What is the treatment for viral meningitis?

A
  • Self-limiting disease, therefore treatment is usually not needed.
67
Q

When does fungal meningitis occur?

A
  • Usually requires immunosupression.
68
Q

What are the most common causes of bacterial meningitis for the different subgroups in the population?

A
  • Neiserria Meningitidis. Most common cause in adolescents.
  • Streptococcus Pneumoniae. Most common cause in immunocompetent adults.
  • Listeria meningitidis. Most common cause in people over 60 and people who are immunosupressed.
69
Q

What is the management for bacterial meningitis?

A

Immediate blood culture.

CSF if possible (ICP not raised).

All patients receieve IMMEIDATE cefotaxime.

Patients over 50/immunocompromised also receive amoxicillin to ensure there is coverage of listeria monocytogenes.

70
Q

What is the CSF composition in patients with bacterial meningitis?

A

Bacterial:

  • Cloudy.
  • Raised protein.
  • Lowered glucose.
  • Neutrophil predominant.
71
Q

What is the CSF composition in patients with viral meningitis?

A
  • Clear.
  • Normal protein/glucose
  • Lymphocyte predominant.
72
Q

What is the CSF composition of patients with fungal meningitis?

A
  • Turbid.
  • Raised protein.
  • Low glucose.
  • Lymphocytes predominant.
73
Q

What are the symtpoms of meningitis?

A
  • Stiff neck.
  • Photophobia.
  • Fever.
  • Headache/altered consciousness (raised ICP).
74
Q

What is encephalitis?

A
  • Inflammation of the brain parenchyma causing neurological dysfunction.
75
Q

What is the presentation of encephalitis?

A

ACUTE ONSET:

  • Fever.
  • Altered mental status.
  • Focal neurological abnormality.
  • Seizure.
76
Q

What are the first line investigations for encephalitis?

A
  • LP. Find causative organism.
  • MRI brain.
77
Q

What is the most common cause of encephalitis?

A
  • HSV (Herpes simplex virus).
78
Q

What is the intial treatment for encephalitis?

A
  • Aciclovir (until confirmed not due to HSV).
  • ICP management (raise bed head to 30 degrees).
79
Q

What is cauda equina syndrome?

A

Compression of the cauda equina (spinal extension) due to disc herniation or vertebral fracture.

80
Q

What are the symptoms and signs of cauda equina syndrome?

A

Symptoms:

  • Bladder dysfunction.
  • Bilateral sciatica (pain in lower back/buttocks).
  • Saddle anasthesia (numbness in lower back and buttocks).

Signs:

  • Lower limb weakness/numbness.
  • Reduced anal tone.
81
Q

What investigation is used in suspected Cauda Equina syndrome?

A
  • MRI lower back.
82
Q

What is the treatment for cauda equina syndrome?

A
  • Neurosurgical decompression.
83
Q

What is the typical presentation of spinal cord compression?

A
  • Hemisensory loss or hemiparesis.
84
Q

What are some potential causes of spinal cord compression?

A
  • Spine trauma.
  • Vertebral compression fracture.
  • Vertebral disc herniation.
  • Spinal cord tumour.
  • Infection.
85
Q

What is the management of spinal cord compression (investigations/treatment)?

A

Investigation:

  • MRI spine.

Treament:

  • Immobilise spine.
  • Neurosurgical decompression.
86
Q

What is brown-sequard syndrome?

A
  • Damage to one side of the spinal cord.
87
Q

What is the clinical presentation of Brown-sequard syndrome? Which spinal tracts are involved in each symptom?

A
  • Ipsilateral loss of vibration/proprioception below level of lesion. DORSAL COLUMN.
  • Ipsilateral paralysis below level of lesion. CORTICOSPINAL TRACT.
  • Contralateral loss of pain +temperature sensation 1-2 segments below level of lesion. SPINOTHALAMIC TRACT.
88
Q

What is the management of Brown Sequard syndrome (Investigations/treatment)?

A
  • MRI spine.
  • Treat with neurosurgical decompression;.
89
Q

What is the function, level of decussation, and location of the following tracts within the spinal cord:

  • Corticospinal tract?
  • Spinothalamic tract?
  • Dorsal column?
A
  • Corticospinal tract. Motor innervation. One lateral and one ventral (anterior). Decussate at level of spinal cord entry.
  • Spinothalamic tract. Pain + temperature sensation. Ventral. Decussate 1-2 levels above level of exit from the spinal cord.
  • Dorsal colum. Proprioception and vibration. Dorsal. Decussate at level of spinal cord entry.
90
Q

What is Parkinson’s disease?

A
  • A chronic progressive neurological disorder.
  • Caused by loss of dopaminergic neruons in the substantia nigra.
91
Q

What is the clinical presentation of Parkinson’s disease?

A
  • Resting tremor (“pill-rolling tremor”).
  • Bradykinesia.
  • Postural instability.
  • Reduced facial expression.
92
Q

What is the treatment for Parkinson’s disease?

A
  • L-DOPA/Levodopa (dopamine precursor).
93
Q

What is trigeminal neuralgia?

A
  • Facial pain distributed to one or more regions of the face supplied by the facial nerve (CN VII).
94
Q

What is the treatment for trigeminal neuralgia?

A
  • Carbamazepine (an anti-convulsant).
95
Q

What is a tension headache?

A
  • Common, every-day headache.
  • Bilateral, like a band around the head.
96
Q

What is the treatment for tension headache?

A
  • Ibuprofen/paracetamol.
  • If chronic (more than 7 headache days a month) consider use of amitriptyline.
97
Q

How does a cluster headache present?

A
  • Attack of severe pain localised to unilaterally to the orbital/temporal area.
  • Occur in cluster periods.
98
Q

What is the treatment for cluster headache?

A

Acute attack - Ibuprofen/paracetamol.

Ongoing management - verapamil (ACEI).

99
Q

What the presentation of migraine?

A
  • Chronic episodic headaches
  • Often assocaited with nausea/vomiting.
  • If with affects on vision, the migraine is WITH AURA.
100
Q

What is the treatment for migrane?

A
  • Topiramate (anti-convulsant) for long-term prevention.
101
Q

What are the symptoms of giant cell arteritis?

A
  • Scalp tenderness.
  • Amaurosis Fugax (“curtian down over eye”)
  • Headache
102
Q

How is giant cell arteritis diagnosed?

A

First line: Ultrasonography of the temporal artery.

GS: Temporal artery biopsy. Will show signs of inflammation.

103
Q

What is the treatment for GCA?

A

Immediate administration of high dose prednisolone.

104
Q

What is the histological presentation of GCA on temporal artery biopsy?

A
  • Granulomatous inflammation.
105
Q

What is trigeminal neuralgia?

How does it present?

A

Facial pain in one or more divisions of the facial nerve.

Presents with sharp stabbing intense pain.

106
Q

What is the treatment for trigeminal neuralgia?

A
  • Carbamazepine (anti-convulsant - sodium channel blocker).
107
Q

What is Sjogren’s syndrome?

What coonditions is it associated with?

A
  • An autoimmune disorder of the salivary glands.
  • Characterised by dry eyes and a dry mouth.

Associated with SLE, RA, systemic sclerosis etc. (other autoimmune disorders).

Phase 2 v2 (14 decks)

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