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Year 3 - Neurology > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Headache - potential relieving and exacerbating factors

A

Posture

headache behaviours (avoiding light, loud noises etc.)

Valsalva (coughing, sneezing etc.) may make it worse - red flag

Diurnal variations - NB, if someone is being woken up BY their headache, this is a big red flag and could suggest raised ICP. Need to ascertain whether they are waking up with a headache or being woken by it

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2
Q

Headache red flags

A

New onset in someone >55 yrs

Known/previous malignancy

IC/IS patients

Early morning headaches/being woken by headache

Exacerbated by valsalva

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3
Q

Men/Women get migraines more commonly

On average, how often does a migraine sufferer have an attack?

A

Women more commonly get migraines (1:2.5)

On average, migraines occur once a month

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4
Q

According to the International Headache Society (IHS), what are the criteria for a migraine (without aura)?

A

A. At least five attacks fulfilling criteria B-D

B. Headache attacks lasting 4-72 hr (untreated or unsuccessfully treated)

C. Headache has at least two of the following four characteristics:

  • unilateral location
  • pulsating quality
  • moderate or severe pain intensity
  • aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)

D. During headache at least one of the following:

  • nausea and/or vomiting
  • photophobia and phonophobia

E. Not better accounted for by another ICHD-3 diagnosis.

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5
Q

What neurotransmitter is released in migraine pathophysiology?

What effect does this have?

What chemicals are released by the brain?

A

Serotonin is released due to changes in the brain causing stress

Serotonin causes blood vessels in the brain to either constrict or dilate, depending on the location/amount of serotonin released

This results in dilatation of cranial blood vessels and the release of Substance P, Neurokinin A and CGRP which irritate the nerves and vasculature, resulting in pain

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6
Q

Once released, what locations in the brain do chemicals affect predominantly to cause migraine symptoms?

A

Substance P, Neurokinin A and CGRP predominantly affect an area known as the “Migraine Centre”, which is comprised of the Dorsal Raphe Nucleus and the Locus Coeruleus

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7
Q

What % of people with migraines get ‘aura’?

Define ‘aura’

A

20%

‘Aura’ is defined as a fully reversible visual, sensory, motor or language symptom, and can last between 20-60 mins. Visual disturbance is the most common form of aura

Headaches typically occur less than an hour after the appearance of aura

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8
Q

What are some of the triggers of migraine?

A

Lack of sleep

Dietary causes (red wine, cheese etc.)

Stress

Hormonal influences e.g. menstruation

Physical exertion

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9
Q

Migraine - pharmacological management in the acute setting

A

NSAIDs (Aspirin, Naproxen, Ibuprofen) +/- anti-emetic to be taken as early as possible (60% reduction in headaches at 2 hours)

Triptans (5HT agonists, Rizatriptan, Frovatriptan) to be taken at the start of the headache. Efficacy is similar to that of NSAIDs, however they are expensive!

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10
Q

Migraine - pharmacological management as prophylaxis

A

Used if a patient is having 3+ attacks a month, or if v. severe

Each drug must be trialed for a minimum of 4 months and “start low, go slow”

Propranolol (beta blocker) - reduction in migraine frequency in 60-80% of patients

Topiramate (Carbonic Anhydrase Inhibitor) - poor side effect profile

Amitriptyline - mechanism of action is unclear and there are a lot of side effects

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11
Q

Migraine - non-pharmacological management options

A

Setting realistic goals

Avoiding triggers (can be identified with headache diaries)

Relaxation/stress management

Lifestyle

  • Diet
  • Hydration – at least 2 litres a day and decrease caffeine
  • Regular exercise
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12
Q

What’s the headache condition? How is it best managed?

Presents with a pressing, tingling quality

Pain is mild-moderate and experienced bilaterally

Absence of N+V, photophobia and phonophobia

A

Tension-Type headache

Best managed with relaxation, reassurance and if severe can use antidepressants (dothiepin/amitriptyline)

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13
Q

What group of headache disorders are characterised by the following symptoms? What are the 4 main types of this disorder?

Unilateral, trigeminal distribution of pain

Occurs in association with prominent ipsilateral cranial autonomic features e.g. ptosis, miosis, nasal stuffiness, tearing, eyelid oedema

A

Trigeminal autonomic cephalgias (TACs)

4 main types

  • Cluster headaches
  • Paroxysmal hemicrania
  • Hemicrania continua
  • SUNCT
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14
Q

What’s the headache condition? How is it best managed

Who: Men>women, age 30s-40s

When: Circadian and seasonal variations

Features: severe unilateral headache lasting 45-90 mins, 1-8 a day and bouts may last weeks to months

A

Cluster headache (form of TAC)

Acutely managed with high flow O2 for 20 mins and subcutaneous sumatriptan, 6mg

Managed in the longer term with steroids and verapamil for prophylaxis

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15
Q

What’s the headache condition? How is it best treated?

Who: Women>Men, age 50s-60s

Features: severe unilateral headache with accompanying unilateral autonomic features lasting 10-30 mins, occurring 1-40 a day

A

Paroxysmal hemicrania (form of TAC)

Absolute response to indomethacin

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16
Q

What does SUNCT stand for? How is it treated?

A

S - short duration (15-120 seconds)

U - unilateral

N - neuralgiaform headache

C - conjunctival injections

T - tearing

Treatment is with either lamotrigine or gabapentin

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17
Q

What’s the headache condition? How is it best managed?

Women > Men

Highly associated with obesity

Presents with headache, diurnal variation and morning N+V and occasionally visual loss?

A

Idiopathic Intracranial Hypertension

Treatment is with weight loss, acetazolamide, regular monitoring of visual fields and CSF pressure and, if necessary, ventricular atrial/lumbar peritoneal shunt

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18
Q

Which protein in the brain, the release of which is caused by serotonin, is particularly seen to rise in migraines and cluster headaches?

A

CGRP

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19
Q

What’s the headache condition? How is it best managed?

Who: Women > Men, age 60+

Features: triggered by touch, typically in the area of CN V2/V3, severe stabbing unilateral pain lasting 1-90 seconds. Frequency is 10-100 a day

A

Trigeminal neuralgia

Treatment

  • Carbamazepine
  • Gabapentin
  • Phenytoin
  • Baclofen
  • Surgical management - ablation of the nerve root or decompression
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20
Q

T/F - compared to other tumours in children, brain tumours are exceedingly rare

A

False - brain tumours are the second most common form of tumour in children

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21
Q

What symptoms might a brain tumour present with?

A

Progressive neurological deficit (often missed!)

Motor weakness (45% of patients)

Headaches (54% of patients)

Worse in the morning/wakes patient up

Gets worse on coughing/leaning forward

Associated with vomiting and seizures

Tiptoeing, ataxia in children

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22
Q

Name some of the different ways the brain can herniate.

Which is the most common?

A

Subfalcine herniation - most common

Central herniation

Uncal transtentorial herniation

Tonsilar herniation (causes Cushing’s Triad)

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23
Q

Uh oh! Patient has a tonsillar herniation and is developing Cushing’s Triad!! What’s that again?

Quick, what do you give them?

A

Cushing’s Triad - reduced, irregular breathing + hypertension + bradycardia

Give the patient Mannitol asap (osmotic diuretic)

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24
Q

Tumours arising from astrocytes account for 60% of all brain tumours (2/3rds of which are high grade), and these can be subclassified into grades I-IV.

Which tumour does each grade correspond to?

A

Grade I - Pilocytic, pleomorphic xanthoastrocytoma. Benign, most commonly occurs in children and the treatment of choice is surgery

Grade II - low grade astrocytoma. Pre-malignant, presents with seizures. Treat with surgical resection and follow up with both chemo and radiotherapy

Grade III - anaplastic astrocytoma. Life expectancy is 3-5 years

Grade IV - glioblastoma multiforme (GBM). Most common primary tumour, life expectancy is 15 months

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25
How are high grade (III and IV) malignant astrocytomas best managed?
**Non-curative surgery** to improve survival quality. NB – it is impossible to entirely remove a glioblastoma, unless it is totally contained within a cyst **Post-op radiotherapy + TMZ** (adjuvant temozolomide) (Stupp protocol, NEJM 2005) Other chemo options include PCV (procarbazine, CCNU, vincristine) and carmustine wafers Radiotherapy – side effects include dropping IQ by 10 in children, skin and hair effects and tiredness Immunotherapy – DCVax-L, intends to use the immune system to target the cancer cells
26
When comparing astrocytomas and cancers resulting from oligodendroglial cells (difficult to distinguish on imaging), what is the main difference regarding treatment options? How does this affect survival rates for cancers resulting from oligodendroglial cells?
Main difference - oligodendroglial cell cancers are **chemosensitive** – procarbazine, lomustine, vincristine Use chemo in conjunction with radiotherapy +/- surgery **Median survival of low grade oligodendroglial tumours: 10 years**
27
What is the most common form of brain tumour? How does this affect management?
**Metastases** is the most common form of brain tumour Needs to look elsewhere in the body for the primary
28
What tumour markers should be looked for in a child with ANY midline brain tumour? Why?
Look for Alpha fetoprotein (**AFP**), Human choriogonadotrophin (**beta-HCG**) and Lactate dehydrogenase (**LDH**) If present, this **indicates that the tumour will be** **sensitive to chemotherapy**
29
What do SIGN guidelines state are the indicators for urgent referral for suspicion of brain cancer (4)?
Focal neurological deficit Changes in behaviour Seizures Headache
30
When investigating possible brain cancer, what are the main two imaging modalities used? What are the benefits of each?
CT - quick, easy and good at seeing blood MRI - gives better definition of tissues and _chronic_ bleeds
31
What is the most common _primary_ brain tumour?
**Glioblastoma multiforme** (Grade IV astrocytoma)
32
What grading criteria is used for determining the extent of a resection of brain tumour?
**Simpson's Grading for Extent of Resection (1957)** Grade I (complete removal including underlying bone) - Grade V (simple decompression with or without biopsy)
33
How might an acoustic neuroma present? What underlying genetic condition is it associated with?
Presents with hearing loss, tinnitus and disequilibrium Associated with **neurofibromatosis II**
34
Name 3 tumour markers associated with brain tumours
Alpha fetoprotein (AFP) Human Choriogonadotrophin (beta-HCG) Placental Alkaline Phosphatase (PLAP)
35
What is the likely cause of bacterial meningitis at the following ages... - neonates - children - 10-21 - 21-65 - 65+
Neonates - Listeria, group B strep, E. coli Childern - H. influenzae 10-21 - Neisseria meningitides 21-65 - Strep pneumoniae \> Neisseria meningitides 65+ - Strep pneumoniae \> Listeria
36
If someone has recently undergone neurosurgery or is post-head trauma, what bacterial species are they most at risk of?
Staph aureus S. epidermidis Gram negative bacilli e.g. E. coli
37
95% of patients with bacterial meningitis will have at least 2 of what 4 symptoms?
Headache Fever Neck stiffness Mental change
38
Meningitis - signs and symptoms
Headache Vomiting Pyrexia Neck stiffness Photophobia Lethargy Confusion Rash
39
Neisseria meningitides is found in the throats of healthy carriers but may cause meningococcal meningitis. What causes the symptoms in this condition?
Neisseria bacteria produce an **endotoxin**
40
Bacterial meningitis (community acquired) - acute treatment
**Ceftriaxone IV 2g bd** (or if penicillin-allergic give Chloramphenicol IV) + **Dexamethasone IV 10mg qds** - continue with dexameth. if cause is pneumococcal meningitis, otherwise discontinue (If Listeria cover is required or if the patient is over 60, add **Amoxicillin IV 2g every 4 hours**, or co-trimoxazole if allergic)
41
In a patient with suspected meningitis, what investigations would you perform? How would this change if the patient was septic?
**Bloods** - cultures, FBC, urea, creatinine, LFTs, clotting, procalcitonin/CRP meningococcal and pneumococcal PCR, serology sample and glucose **Throat swab** - bacterial culture **CSF via LP** - opening pressure, microscopy culture and sensitivity, protein, glucose, lactate, meningococcal and pneumococcal PCR Further tests... If patiet is septic, **delay the LP until the patient is stable**
42
How is meningitis classified?
Acute pyogenic (bacterial) Acute aseptic (typically viral) Acute focal suppurative infection (brain abscess, subdural and extradural empyema) Chronic bacterial infection (e.g. due to TB) Acute encephalitis (infection of the brain parenchyma)
43
When assessing a patient with suspected encephalitis, what pathogen are you most concerned about? What questions might you ask a patient to determine if the cause is another pathogen?
Most concerned about **Herpes simplex virus** Current/recent febrile or influenza-like illness? Altered behaviour/cognition? New onset seizures? Focal neurological symptoms? Rash? (chicken pox, enterovirus) Others close to you been ill? (Measles, mumps, influenza) Travel history? Recent vaccinations? Contact with animals (rabies) or fresh water (leptospirosis)? Insect bites? IC/IS? HIV risk factors?
44
Encephalitis - clinical features and investigations
Clinical features * insidious onset * meningismus (stiffness) * stupor, coma * seizures, partial paralysis * confusion, psychosis * speech and memory symptoms Investigations * LP * EEG * MRI
45
What might you do if there has been a delay in assessing a patient with suspected encephalitis?
May begin pre-emptive treatment with **aciclovir** as prompt therapy improves outcomes in cases of H. simplex encephalitis
46
Stroke is not a diagnosis in of itself! What are the three broad classifications of stroke (bonus points for subclassifications!)
**Haemorrhage** * structural abnormality * hypertensive * amyloid angiopathy **Subarachnoid haemorrhage** **Infarct** * cardioembolic * small vessel * atheroembolic * other
47
What important point should be remembered when people arrive at A+E with suspected stroke, regarding correct diagnosis?
A final diagnosis is only made in approx. 2/3rds of patients, meaning that **1/3rd of all stroke presentations are stroke mimics** This highlights the importance of taking a good clinical history
48
What scoring system is used in the emergency room to determine if a patient has likely had a stroke?
**ROSIER score** (recognition of stroke in the emergency room) Score of \> 0 means that a stroke is likely Score of less than or equal to 0 means that the chances of stroke are lower, ubt cannot completely exclude
49
When determining the type of stroke someone has had, what imaging modalities are used and when?
**CT** - bleeds appear bright white, infarcts appear darker. Used in a more acute setting as not great at differentiating between infarcts and chronic bleeds, CT is not sensitive for blood after about 1 week **MRI** - if the patient presents more than 1 week after symptom onset then MRI is the better choice, blood will be reabsorbed and scar, appearing darker
50
What is the prognosis like (independent at 1 year, dead at 30 days, dead at 1 year) for the following 4 types of stroke? (basically, which is the worst?) - POCI - LACI - TACI - PACI
**POCI (posterior circulation infarct)** * independant @ 1 year - 62% * dead @ 30 days - 7% * dead @ 1 year - 19% **LACI (lacunar infarct)** * independant @ 1 year - 60% * dead @ 30 days - 2% * dead @ 1 year - 11% **TACI (total anterior infarct) - worst to have** * independant @ 1 year - **4%** * dead @ 30 days - **39%** * dead @ 1 year - **60%** **PACI (partial anterior infarct)** * independant @ 1 year - 55% * dead @ 30 days - 4% * dead @ 1 year - 16%
51
How does a Total Anterior Circulation Infarct (TACI) present?
Hemiplegia involving at least two of face. arm and leg +/- hemisensory loss Homonymous hemianopia Cortical signs (dysphasia, neglect etc.)
52
How does a Partial Anterior Circulation Infarct (PACI) present?
2/3 features seen in TACI or; isolated cortical dysfunction e.g. dysphasia or; pure motor/sensory signs less severe than in lacunar syndromes
53
How does a Lacunar Circulation Infarct (LACI) present?
Smaller infarcts deeper in the brain (e.g. basal ganglia, thalamus, white matter) and in the brain stem Best prognosis of all the strokes One-sided weakness and sensory loss
54
How does a Posterior Circulation Infarct (POCI) present?
Cranial nerve palsies Slurred speech Dysphagia Double vision Dizziness and unsteadiness
55
For 95% of the population, the right side of the brain deals with ____ and the left side of the brain deals with \_\_\_\_ How does this affect stroke prognosis?
Right side * creativity * music * spatial orientation * artisitic awareness Left side * spoken language * reasoning * numeracy * written language Strokes affecting the **left side of the brain often result in greater disability (language affected)**, whereas if affecting the right side neglect is more likely
56
When dealing with a patient that has a primary intracerebral haemorrhage (i.e. haemorrhagic stroke due to either hypertension or amyoid angiopathy), what single factor is the biggest determinant of subsequent bleeds?
Control of blood pressure
57
Stroke - acute management
Thrombolysis/thrombectomy Imaging, either CT or MRI if later Swallow assessment Nutrition and hydration Antiplatelets Stroke unit care DVT prophylaxis
58
The decision to thrombolyse or not in a patient presenting with a stroke is based on a balance between risks and benefits. What are some of the contributing factors that need to be considered?
Patient age Time since onset Previous haemorrhage or infarct Atrophic changes BP Is the patient diabetic
59
What is the quick screening programme that may indicate if someone is having a stroke?
**FAST** **F - facial weakness**, can they smile/has their eye or mouth drooped **A - Arm weakness**, can they raise both their arms **S - speech problems**, can the person speak clearly T - test all three of the above
60
The type of stroke dictates the best course of action regarding treatment. What is the difference between a cardioembolic and atheroembolic stroke?
Cardioembolic - **fibrin dependent** ("red thrombus") Atheroembolic **platelet dependent** ("white thrombus")
61
Other than imaging with CT or MRI, what other investigations might you perform to determine the type of stroke?
Full lipid profile Blood pressure Carotid scan ECG Also consider 72-hour ECG and/or echocardiogram
62
What is the CHA2DS2VASc score used for?
Used to determine the likelihood of stroke in someone with AF
63
What is the mean pressure of CSF (ICP)? Above what value would be considered abnoramlly high?
10mm Hg \>15mm Hg would be considered abnormal
64
CSF production follows a circardian rythm - when is it at its highest vol and lowest vol? What medication reduces CSF production by more than 50%?
Highest at 2am Lowest at 6pm **Acetazolamide** reduces CSF production
65
Paediatric hydrocephalus can be broken down into congenital and acquired causes. Provide some examples for each category
Congenital * Chiari malformation in spina bifida * Aqueductal stenosis * Dandy-Walker complex * Congenital arachnoid cysts * Atresia of the foramen of Munro Acquired * Haemorrhage * Infection (post meningitis) * Traumatic head injury * Tumour
66
What group typically gets normal pressure hydrocephalus? What triad of symptoms is seen?
Elderly Triad of **ataxia, memory decline and incontinence**
67
What are some of the causes of normal pressure hydrocephalus?
Idiopathic Post-inflammatory - sub-arach. haemorrhage, meningitis, trauma, craniotomy
68
What symptom of normal pressure hydrocephalus is essential to the diagnosis and precedes all other symptoms?
**Ataxia** - difficulty in rising from chair, tendency to fall backwards, broad based shuffling gait
69
Normal pressure hydrocephalus - investigations
Clinical + CT head (shows enlarged ventricles) MRI ICP measurement LP "tap test" Lumbar drainage tests
70
What is a "sunsetting" sign and what might it indicate in children?
Clinical phenomenon - up-gaze paresis with the eyes appearing to be driven downwards, lower portion of the pupil may be covered by the lower eye lid Seen in infants and young children with **raised ICP** e.g. in hydrocephalus
71
What is the difference between a hyperkinetic and hypokinetic movement disorder? Examples of each?
Hyperkinetic = too much movement * tremor * tics * chorea * myoclonus * dystonia Hypokinetic = too little movement * Parkinsonism
72
# Define the following terms... Tremor Tic Chorea Myoclonus Dystonia
Tremor = **rhythmic sinusoidal oscillation** of a body part Tic = **involuntary stereotyped** movements or vocalisations Chorea = **brief, irregular purposeless movements** which flit and flow from one body part to another Myoclonus = **brief, electric-shock like jerks** Dystonia = **abnormal posture** of the affected body part
73
Approach to a patient presenting with tremor - history, examinations and investigations?
History * age of onset * areas affected * precipitating factors/drug or toxin exposure * what makes it better or worse * associated symptoms (neurological and systemic) * family history Examination * examine patient at rest, on posture and during movement * ask patient to write something and copy a spiral * complete physical and neurological examination Investigation * guided by presentation * consider **thyroid function test** and **copper/coeruloplasmin** if young (\<45)
74
Essential tremor (ET) is considered to be the most common movement disorder with a prevalence of 5% in the general population. How does it present (core and secondary criteria)?
Core criteria * **bilateral action tremor** of the hands and forearms * **absence** of other neurological signs * may have isolated tremor with no signs of dystonia Secondary criteria * long duration (\>3 years) * positive family history * benefits in the presence of alcohol
75
Essential tremor - first line treatment
Propranolol then Primidone For severely affected individuals, deep brain stimulation of the ventralis intermedius nucleus
76
When examining a patient complaining of tics, what would you assess?
Are the tics suppressible? Are they motor tics, vocal tics, or both? Are they simple tics, complex tics, or both? Are there any other neurological signs
77
Primary causes of tics include 'simple transient tics of childhood', 'chronic tics of childhood', 'Tourette's syndrome' and 'Adult onset Tourettism'. What are some of the secondary causes of tics?
**Neurodegenerative** * Huntington's * Rett's syndrome * Lesch-Nyhan syndrome * Neuroacanthocythosis * Neuronal brain iron accumulation syndrome **Developmental** * Down Syndrome/other chromosomal abnormalities * Fragile X syndrome * Autism **Structural abnormalities** * post-encephalopathy * basal ganglia lesions **Infection** * Sydenham's chorea (group A beta-haemolytic strep infection during childhood) **Drugs and toxins** * carbon monoxide * cocaine * amphetamines
78
What are some of the diagnostic criteria for Tourette's Syndrome?
Both multiple motor tics and one or more vocal tics must be present Tics must occur many times in a day, nearly every day, or intermittently for a year Age of onset \<18 Exclusion of other obvious secondary causes
79
How is Tourette's Syndrome treated?
Symptomatic treatment - **clonidine, tetrabenazine** Psychopathology, including CBT
80
# Define the following terms... - Copropraxia - Echopraxia - Coprolalia - Echolalia - Palilalia
Copropraxia - production of obscene gestures Echopraxia - copying the movements of others Coprolalia - saying obscene words Echolalia - copying the words of others Palilalia - repetition of the same phrase, word or syllable
81
What are some of the causes of chorea?
Inherited/degenerative * Huntington's Disease * Wilson's Disease * Neuroacanthocythosis * Benign hereditary chorea Autoimmune * SLE * Anti-phospholipid syndrome * Bechet syndrome * Coeliac disease * Sydenham's chorea * Hashimoto's Infectious * HIV Drugs * Dopamine-receptor blocking drugs, levodopa, stimulants, oral contraceptive pill, anticonvulsants Paroxysmal Chorea * Parkinson's Disease Metabolic * Chorea gravidarum, glucose, thyroid, parathyroid, sodium, magnesium metabolism
82
Huntington's Disease - mode of inheritence What is the telltale genetic abnormality seen and what chromosome is it found on?
Autosomal dominant **CAG triplet-repeat expansion** (40 or more = disease, 35 or less = no disease, 36-39 is uncertain) affecting the **Huntingtin gene on chromosome 4** Greater the number of repeats, the earlier the disease affects the patient
83
What are some of the causes of symptomatic myoclonus with encephalopathy?
Liver failure Renal failure Drugs (alcohol, lithium) Toxins (lead) Post hypoxia
84
What are some of the causes of symptomatic myoclonus without encephalopathy?
Plus dementia - Alzheimer's, Lewy Body Dementia, Creuztfeldt-Jakob disease Plus Parkinsonism - corticobasal degeneration, multiple system atrophy, spinocerebellar ataxias Focal/segmental - spinal cord, root, plexus injury Other - Whipple disease, Coeliac disease, paraneoplastic, drugs
85
Juvenile Myoclonic Epilepsy - when does it begin, what is it typically associated with, when are symptoms worse, what does an EEG show and how is it treated?
Onset is in teenage years Associated with sleep deprivation and alcohol Symptoms are typically worst in the mornings EEG shows characteristic 3-5Hz polyspike and wave discharges **Sodium valproate** and **levetiracetam** are effective and are usually required long-term, note that carbamazepine can aggrevate the condition
86
50-60% of patients with Young Onset Primary Dystonia have what mutation in what chromosome? How is this inherited?
Mutation of the **DYT1 gene on chromosome 9q** due to a GAG deletion **Autosomal dominant** inheritance
87
What drug is trialled in all patients with young onset dystopia? Why?
**Levodopa** is trialled in all patients because **dopa-responsive dystonia** is a differential for young onset dystopia
88
What treatment plays an important role in managing focal dystonias?
Botulinum toxin
89
When getting a history for someone that has had a fall (suspected seizure), what questions should be asked regarding onset, the event itself and what happened afterwards?
Onset * what were they doing * did they feel light-headed or have any other syncopal symptoms * what did they look like? * pallor, breathing * posturing of limbs, head turning Event * type of movements * tonic phase, clonic movements * carpopedal spasms, rigor * where they responsive and aware throughout Afterwards * speed of recovery * did they experience any sleepiness or disorientation * were there any lasting deficits
90
What investigation does EVERYONE that has a new seizure get?
ECG
91
EEGs are a good/bad test. Why?
EEGs are a **bad test** Epileptic patients may have a normal EEG, and 1/5 will have an abnormal EEG but with no pathology
92
What is the only reason to do an EEG?
To confirm a non-convulsive status in a patient that has had a seizure (convulsive seizures are more common and more dangerous)
93
Someone presents with a "seizure", but what are some of the conditions this may be, other than epilepsy?
Syncope Non-epileptic attack disorder (pseudoseizures, psychogenic non-epileptic attacks) Panic attacks/hyperventilation attacks Sleep phenomena TIAs Migraine Hypoglycaemia Parasomnias Paroxysmal movement disorders etc. etc.
94
When counselling a patient that has had a seizure, what are some of the important points to mention?
Seizure doesn't always = epilepsy. Seizure prevalence is 2-5%, epilepsy prevalence is 0.5% Warn of the risk of recurrence **Driving and safety** 1st seizure: **can't drive a car for 6 months, or HGV/PCV for 5 years** If newly diagnosed with epilepsy: **must be completely seizure free for 1 year** **before you can drive, with or without anti-epileptic medication**. If driving **HGV/PCV,** **must be seizure free for 10 years WITHOUT anti-epileptic drugs**
95
What is the difference between a focal and generalised epileptic seizure? How long do epileptic seizures typically last?
Focal = affects one part of the brain (NB - focal epilepsies can also cause generalised seizures!) Generalised = affects a larger part of the brain Epileptic seizures are **usually brief (seconds-minutes)** - anything more than 10 mins is pathological
96
Generally speaking, generalised epilepsy tends to present ____ while partial/focal epilepsy tends to present \_\_\_\_
**Generalised** epilepsy tends to present in **childhood and adolescence** **Partial/focal** epilepsy tends to present **\>50 years old**
97
What is the treatment of choice for _generalised_ seizures? What is the side-effect and what is the alternative?
**Sodium valproate** is the treatment of choice, but it is **teratogenic** so **Lamotrigine** can be used as an alternative. Choose ONE as if both are used at the same time this may cause Steven Johnson Syndrome
98
What is the treatment of choice for focal/partial onset epilepsy? What is the main downside?
**Carbamazepine** is the main drug of choice, however **it causes other drugs to be less effective** e.g. oral contraceptive, chemo etc. **Lamotrigine** can also be used as an alternative
99
What are the outcomes like with Anti-Epileptic Drugs (AEDs)?
55% are seizure free on monotherapy 10% are seizure free on polytherapy 35% have **"drug resistant epilepsy"**
100
What are some of the add on drugs that can be used to treat partial/focal epilepsy if initial therapy isn't sufficient?
Gabapentin Tiagabine Pregabalin Zonisamide Clonazepam/Clobazam Older drugs - Phenytoin, Phenobarbitone, Primidone
101
What drug should NEVER be given to manage generalisd epileptic seizures?
**Carbamazepine** - can make seizures worse
102
Phenytoin, Sodium Valproate and Carbamazepine are known as "old" anticonvulsant medications. What are some of the newer ones?
Lamotrigine - well tolerated but takes a long time to titrate up **Levetiracetam** - v. popular, few interactions and well tolerated Topiramate - sedation, dysphasia and weight loss Gabapentin, Pregabalin
103
In women with epilepsy that have been given anticonvulsants, what needs to be kept in mind?
Some anticonvulsants induce hepatic enzymes, meaning **efficacy of contraception is affected!!!** Combined oral contraceptive may be affected Progesterone-only pill shouldn't be used Depot progesterone requires more frequent dosing Progesterone implants are not effective Need increased dose of morning after pill
104
What is status epilepticus?
Recurrent epileptic seizures without full recovery of consciousness lasting more than 30 minutes Types * Generalised convulsive SE * Non-convulsive * Epilepsia partialis continua (continual focal seizures but consciousness is preserved)

Year 3 - Neurology (7 decks)

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