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A-CCC > GP- neuro > Flashcards

GP- neuro Flashcards

1
Q

epilepsy definition

A

Epilepsy is a condition characterised by seizures. Seizures are transient episodes of abnormal electrical activity in the brain.

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2
Q

types of seizures seen in adults

A

Generalised tonic-clonic seizures
Partial seizures (or focal seizures)
Myoclonic seizures
Tonic seizures
Atonic seizures

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3
Q

The types of seizures more common in children include:

A

Absence seizures
Infantile spasms
Febrile convulsions

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4
Q

describe the features of a partial /focal seizure

A
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5
Q

describe the features of a partial /focal seizure

A
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6
Q

describe the features of myoclonic seizures

A

Myoclonic seizures present with sudden, brief muscle contractions, like an abrupt jump or jolt. They remain awake. Myoclonic seizures can occur as part of juvenile myoclonic epilepsy in children.

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7
Q

describe the features of tonic seizures

A

Tonic seizures involve a sudden onset of increased muscle tone, where the entire body stiffens. This results in a fall if the patient is standing, usually backwards. They last only a few seconds, or at most a few minutes.

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8
Q

describe the features of atonic seizures

A

Atonic seizures (causing “drop attacks”) involve a sudden loss of muscle tone, often resulting in a fall. They last only briefly, and patients are usually aware during the episodes. They often begin in childhood. They may be indicative of Lennox-Gastaut syndrome.

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9
Q

describe the features of absence seizures

A

Absence seizures are usually seen in children. The patient becomes blank, stares into space, and then abruptly returns to normal. During the episode, they are unaware of their surroundings and do not respond. These typically last 10 to 20 seconds. Most patients stop having absence seizures as they get older.

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10
Q

infantile spasms description, investigation and treatment

A

Infantile spasms are also known as West syndrome. It is a rare (1 in 4,000) disorder starting at around six months of age. It presents with clusters of full-body spasms. Hypsarrhythmia is the characteristic EEG finding. It is associated with developmental regression and has a poor prognosis. Treatment is with ACTH and vigabatrin.

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11
Q

febrile convulsions features

A

Febrile convulsions are tonic-clonic seizures that occur in children during a high fever. They are not caused by epilepsy or other pathology (e.g., meningitis or tumours). Febrile convulsions occur in children aged between 6 months and 5 years. Febrile convulsions do not usually cause any lasting damage. One in three will have another febrile convulsion. They slightly increase the risk of developing epilepsy.

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12
Q

differentials to seizures

A
  • Vasovagal syncope (fainting)
  • Pseudoseizures (non-epileptic attacks)
  • Cardiac syncope (e.g., arrhythmias or structural heart disease)
  • Hypoglycaemia
  • Hemiplegic migraine
  • Transient ischaemic attack
  • alcohol/drug use
  • metabolic disorder/ electrolyte abnormalities
  • brain bleed
  • infection: sepsis, encephalitits, meningitis
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13
Q

investigations in epilepsy

A
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14
Q

management of epilepsy

A

Other less commonly used anti-epileptic drugs to be aware of include:
* Carbamazepine
* Phenytoin
* Topiramate

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15
Q

sodium valproate MOA and SE

A
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16
Q

status epilepticus definition

A

Status epilepticus is a medical emergency defined as either:

  • A seizure lasting more than 5 minutes
  • Multiple seizures without regaining consciousness in the interim
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17
Q

status epilepticus management

A

Consider thiamine/glucose IV if alcoholism suspected influence

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18
Q

definition of stroke and different types

A
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19
Q

Ischaemia refers to

A

inadequate blood supply

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20
Q

Infarction refers to

A

tissue death due to ischaemia

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21
Q

The blood supply to the brain may be disrupted by:

A

A thrombus or embolus
Atherosclerosis
Shock
Vasculitis

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22
Q

Anatomy of blood supply to the brain: circle of Willis

A
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23
Q

TIA definition and symptoms

A
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24
Q

Crescendo TIAs definition

A

two or more TIAs within a week and indicate a high risk of stroke.

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25
Q

Stroke presentation

A
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26
Q

Risk factors for stroke

A
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27
Q

fast tool

A

F – Face
A – Arm
S – Speech
T – Time (act fast and call 999)

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28
Q

management of TIA

A
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28
Q

which scoring tool is used for stroke

A

The ROSIER tool (Recognition Of Stroke In the Emergency Room) gives a score based on the clinical features and duration. Stroke is possible in patients scoring one or more.

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29
Q

investigations for TIA

A
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30
Q

secondary prevention in TIA

A
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31
Q

management of stroke

A
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32
Q

assessment for underlying causes in TIA and stroke

A
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33
Q

secondary prevention of stroke

A
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34
Q

what can be given as secondary prevention of stroke if clopidogrel is contraindicated

A
  • aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated, but treatment is no longer limited to 2 years’ duration
  • MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated, again with no limit on duration of treatment
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35
Q

absolute contraindications for thrombolysis in stroke

A
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36
Q

rehab in stroke

A
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37
Q

first line investigation for suspected stroke and result differences between ischaemic and haemorrhagic strokes

A
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38
Q

Essential tremor definition

A

Essential tremor (previously called benign essential tremor) is an autosomal dominant condition which usually affects both upper limbs

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39
Q

essential tremor features

A
  • postural tremor: worse if arms outstretched
  • Fine tremor (6-12 Hz)
  • Symmetrical
  • More prominent with voluntary movement
  • Worse when tired, stressed or after caffeine
  • Improved by alcohol
  • Absent during sleep

most notable in the hands but can affect other areas, for example, causing a head tremor, jaw tremor and vocal tremor.

most common cause of titubation (head tremor)

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40
Q

essential tremor differentials

A

Benign essential tremor is diagnosed clinically based on the presenting features after excluding other causes. The key differential diagnoses of a tremor are:

  • Parkinson’s disease
  • Multiple sclerosis
  • Huntington’s chorea
  • Hyperthyroidism
  • Fever
  • Dopamine antagonists (e.g., antipsychotics)
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41
Q

essential tremor management

A

There is no definitive treatment for benign essential tremor. The tremor is not harmful and does not require treatment if it is not causing functional or psychological problems.

Medications that may improve symptoms are:

Propranolol (a non-selective beta blocker)
Primidone (a barbiturate anti-epileptic medication)

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42
Q

Multiple sclerosis (MS) is

A

Multiple sclerosis (MS) is a chronic and progressive autoimmune condition involving demyelination in the central nervous system. The immune system attacks the myelin sheath of the myelinated neurones.

43
Q

Multiple sclerosis typically presents in

A

Multiple sclerosis typically presents in young adults (under 50 years) and is more common in women.

44
Q

MS pathophysiology

A
45
Q

causes of the multiple sclerosis

A

The cause of the multiple sclerosis is unclear, but there is growing evidence that it may be influenced by:

Multiple genes
Epstein–Barr virus (EBV)
Low vitamin D
Smoking
Obesity

46
Q

Onset of MS

A

Symptoms usually progress over more than 24 hours. Symptoms tend to last days to weeks at the first presentation and then improve. There are many ways MS can present, depending on the location of the lesions.

47
Q

Summary of MS symptoms

A
48
Q

most common presentation of multiple sclerosis and its key features

A
49
Q

differential diagnosis to optic neuritis

A

Other causes of optic neuritis include:

Sarcoidosis
Systemic lupus erythematosus
Syphilis
Measles or mumps
Neuromyelitis optica
Lyme disease

Patients presenting with acute loss of vision need urgent ophthalmology input. Optic neuritis is treated with high-dose steroids. Changes on an MRI scan help to predict which patients will go on to develop MS.

50
Q

eye movement abnormalities in optic neuritis

A
51
Q

what are focal neurological symptoms in MS?

A
52
Q

Ataxia is

A

Ataxia is a problem with coordinated movement. It can be sensory or cerebellar.

53
Q

Sensory ataxia is due to…
this leads to..
a lesion in the… can cause sensory ataxia

A

Sensory ataxia is due to loss of proprioception, which is the ability to sense the position of the joint (e.g., is the joint flexed or extended).

This results in a positive Romberg’s test (they lose balance when standing with their eyes closed) and can cause pseudoathetosis (involuntary writhing movements).

A lesion in the dorsal columns of the spine can cause sensory ataxia.

54
Q

Cerebellar ataxia results from…indicating a …lesion.

A

Cerebellar ataxia results from problems with the cerebellum coordinating movement, indicating a cerebellar lesion.

55
Q

MS investigations

A
56
Q

MS management

A
57
Q

disease pattern in MS

A
58
Q

Causes of headaches

A
59
Q

Red flags in a headache

A

Key red flags associated with a headache, indicating a possible serious underly cause, include:

  • Fever, photophobia or neck stiffness (meningitis, encephalitis or brain abscess)
  • New neurological symptoms (haemorrhage or tumours)
  • Visual disturbance (giant cell arteritis, glaucoma or tumours)
  • Sudden-onset occipital headache (subarachnoid haemorrhage)
  • Worse on coughing or straining (raised intracranial pressure)
  • Postural, worse on standing, lying or bending over (raised intracranial pressure)
  • Vomiting (raised intracranial pressure or carbon monoxide poisoning)
  • History of trauma (intracranial haemorrhage)
  • History of cancer (brain metastasis)
  • Pregnancy (pre-eclampsia)
  • sudden-onset headache reaching maximum intensity within 5 minutes - ‘thunderclap’
  • new-onset neurological deficit
  • new-onset cognitive dysfunction
  • change in personality
  • impaired level of consciousness
  • compromised immunity, caused, for example, by HIV or immunosuppressive drugs
  • a substantial change in the characteristics of their headache

Fundoscopy for papilloedema is an important. Papilloedema suggests raised intracranial pressure, which may be due to a brain tumour, benign intracranial hypertension or an intracranial bleed.

TOM TIP: Asking specifically about red flags demonstrates that you are thinking about serious causes. This will score extra points in OSCEs and help you document well when seeing patients.

60
Q

Tension headaches symptoms, causes and management

A
61
Q

Secondary headaches presentation and cause

A

Secondary headaches give a similar presentation to a tension headache but with a clear cause, such as:

Infections (e.g., viral upper respiratory tract infection)
Obstructive sleep apnoea
Pre-eclampsia
Head injury
Carbon monoxide poisoning

62
Q

Sinusitis headache presentation and management

A
63
Q

Medication-overuse headache presentation and management

A

Medication-overuse headache (also called analgesic headache) is a headache caused by frequent analgesia use. It gives similar non-specific features to a tension headache.
Withdrawal of the analgesia is important in treating the headache, although this can be challenging in patients with long-term pain.

64
Q

Hormonal headache cause, presentation and management

A
65
Q

Cervical spondylitis, cause, presentation and management

A

Cervical spondylosis is an extremely common condition that results from osteoarthritis.

It most commonly presents as neck pain although referred pain may mimic headaches etc.

Complications include radiculopathy and myelopathy.

66
Q

Trigeminal neuralgia definition, causes, symptoms and management

A
67
Q

NICE Clinical Knowledge Summaries list the following as red flag symptoms and signs suggesting a serious underlying cause for trigeminal neuralgia:

A
  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  • Optic neuritis
  • A family history of multiple sclerosis
  • Age of onset before 40 years
68
Q

Temporal arteritis presentation

A

Typically patient > 60 years old
Usually rapid onset (e.g. < 1 month) of unilateral headache
Jaw claudication (65%)
Tender, palpable temporal artery
Raised ESR

69
Q

Diagnosis of temporal arteritis

A
70
Q

temporal arteritis defintion and key complication

A

Giant cell arteritis (GCA) is also known as temporal arteritis. It is a type of systemic vasculitis affecting the medium and large arteries. There is a strong link with polymyalgia rheumatica. It is more common in older white patients.

The key complication of giant cell arteritis is vision loss, which is often irreversible.

71
Q

temporal arteritis management

A
72
Q

temporal arteritis complications

A

Steroid-related complications (e.g., weight gain, diabetes and osteoporosis)
Visual loss
Cerebrovascular accident (stroke)

73
Q

cluster headaches presentation

A
74
Q

cluster headaches management

A
75
Q

migraines: 4 main types and the population it affects the most

A
76
Q

five stages of migraine sand migraine features

A
77
Q

describe the symptoms of an aura

A
78
Q

hemiplegic migraine presentation and differential diagnoses

A
79
Q

migraines triggers

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

80
Q

migraines acute attack management

A
81
Q

triptans drug class, MOA, how they can be taken to treat migraines, main contraindications

A
82
Q

prophylaxis treatment for migraines

A
83
Q

Parkinson’s disease definition

A

Parkinson’s disease is a condition where there is a progressive reduction in dopamine in the basal ganglia, leading to disorders of movement. The symptoms are characteristically asymmetrical, with one side of the body affected more. The typical patient is an older man, around 70 years old, with a gradual onset of symptoms.

84
Q

Parkinson’s classic triad of features

A
85
Q

Parkinson’s pathophysiology

A

The basal ganglia are a group of structures situated near the centre of the brain. They are responsible for coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patterns.

Dopamine plays an essential role in the basal ganglia function. Patients with Parkinson’s disease have a slow but progressive drop in dopamine production.

86
Q

Parkinson’s features

A
87
Q

Parkinson’s vs essential tremor

A
88
Q

what are Parkinson’s plus syndromes and their features?

A
89
Q

How is Parkinson’s diagnosed?

A

Parkinson’s disease is diagnosed clinically based on the history and examination findings. The diagnosis should be made by an experienced specialist. The NICE guidelines (2017) recommend the UK Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria.

90
Q

Parkinson’s management: first line treatment plus when second line. Explain how each drug’s effect on Parkinson’s symptoms

A

Parkinsons disease should only be diagnosed, and management initiated, by a specialist with expertise in movement disorders.

Patients may describe themselves as “on” when the medications are acting, and they are moving freely, and “off” when the medications wear out, they are experiencing symptoms and their next dose is due.

The treatment options are:

  • Levodopa (combined with peripheral decarboxylase inhibitors)
  • COMT inhibitors
  • Dopamine agonists
  • Monoamine oxidase-B inhibitors
91
Q

Levodopa drug class, main side effect plus others, how is it taken?

A

Levodopa is synthetic dopamine taken orally

The main side effect of levodopa is dyskinesia. Dyskinesia refers to abnormal movements associated with excessive motor activity

92
Q

Amantadine drug class and side effects

A

Amantadine is a glutamate antagonist that may be used to manage dyskinesia associated with levodopa.

  • mechanism is not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses
  • side-effects include ataxia, slurred speech, confusion, dizziness and livedo reticularis
93
Q

What is COMT used for? Drug class

A

COMT Inhibitors (e.g., entacapone) are inhibitors of catechol-o-methyltransferase (COMT).
The COMT enzyme metabolises levodopa in both the body and brain.
Entacapone is taken with levodopa (and a decarboxylase inhibitor) to slow the breakdown of the levodopa in the brain. It extends the effective duration of the levodopa.

94
Q

Dopamine receptor agonists examples, what are they used for? Notable side effects

A

Dopamine agonists mimic the action of dopamine in the basal ganglia, stimulating the dopamine receptors. They are less effective than levodopa in reducing symptoms. They are typically used to delay the use of levodopa, then used in combination with levodopa to reduce the required dose.

notable side effect with prolonged use:
* ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis. The Committee on Safety of Medicines advice that an echocardiogram, ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored
* potential to cause impulse control disorders and excessive daytime somnolence
* more likely than levodopa to cause hallucinations in older patients.
* Nasal congestion and postural hypotension are also seen in some patients

Examples are:

  • Bromocriptine
  • Pergolide
  • Cabergoline
95
Q

Monoamine oxidase-B inhibitors MOA, examples, how is it used?

A

Monoamine oxidase-B inhibitors block the action of monoamine oxidase-B enzymes, helping to increase the circulating dopamine. Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline.

Monoamine oxidase-B is more specific to dopamine. They are typically used to delay the use of levodopa, then in combination with levodopa to reduce the “end of dose” worsening of symptoms.

Examples are:

  • Selegiline
  • Rasagiline
96
Q

Antimuscarinics MOA, examples and how is it used in relation to Parkinson’s

A
  • block cholinergic receptors
  • now used more to treat drug-induced parkinsonism rather than idiopathic Parkinson’s disease
  • help tremor and rigidity
  • e.g. procyclidine, benzotropine, trihexyphenidyl (benzhexol)
97
Q

Motor neurone disease deifnition

A

Motor neurone disease is a term that encompasses a variety of specific diseases affecting the motor nerves. Motor neurone disease is a progressive, eventually fatal condition where the motor neurones stop functioning.

98
Q

types of motor neurone disease

A

There is no effect on the sensory neurones. Sensory symptoms suggest an alternate diagnosis.

Amyotrophic lateral sclerosis (ALS) is the most common and well-known type of motor neurone disease. Stephen Hawking had amyotrophic lateral sclerosis.

99
Q

pathophysiology of motor neurone disease

A
100
Q

presentation of motor neurone disease

A
101
Q

Signs of lower motor neurone disease:

A
102
Q

Signs of upper motor neurone disease:

A
103
Q

diagnosis of motor neurone disease

A

The diagnosis needs to be made very carefully. It is based on the clinical presentation after excluding other conditions. It should only be made by a specialist when there is certainty. The diagnosis is often delayed, causing stress.

104
Q

Management of motor neurone disease

A

A-CCC (9 decks)

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