D-E

Question 1

What is Depression?

Answer 1

ICD10: depressed mood, anhedonia, low energy, fatigue leading to impaired personal and social function.

Other features include low concentration and attention, low self esteem and confidence, guilt and unworthiness, bleak view of future, disturbed sleep and appetite, acts of self harm and suicide.

Question 2

What is episode classification in depression?

Answer 2

· Mild: 2 cardinal and 2 other features for over 2wk

· Moderate: episode 2 cardinal and 3-4 other features for over 2ek

· Severe: 3 cardinal and 4+ other features for over 2wk

Question 3

What is the aetiology of depression?

Answer 3

Genetic: positive Foxx. Parental mental health, unemployment, poverty, drug abuse in parents, neglect, life events, poor support network, lack of friends, family break up. Systemically, anaemia, post viral syndrome (EBV), hypothyroidism and chronic illness are associated.

? due to reduction in serotonergic transmission in brain to contribute, Reduction of activity in PFC paired with 5HT and NA neuron regulation.

Question 4

What is the epidemiology of depression?

Answer 4

12m prevalence increases with age.

Question 5

What is found in history and exam of a child with depression?

Answer 5

Manifestation in children is affected by developmental stage and ability to identify and express internal emotions. Can be shown by somatization, poor academic performance, being bored, ick or lacking interest, disorganized or reckless behavior, separation anxiety, angry outbursts, alcohol or substance abuse, abuse of other individuals.

Question 6

What are the investigations and management of a child with depression?

Answer 6

CAMHS assessment, bloods (FBC, clotting, TFT and viral screen to seek physiological cause)

Child and family, CBT, IPT, FT. Medical: SSRI, with careful monitoring for suicidal behavior.

Question 7

What are the complications of depression?

Answer 7

Poor school performance, unemployment criminality and drug abuse, self harm (though most self harm is not in clinically depressed children), suicide (3% risk in 10y)

10% recover spontaneously at 3m, 40% first year. 24month 70%.

Question 8

What is the definition of encephalitis?

Answer 8

Inflammation of the brain parenchyma.

Question 9

What is the aetiology of encephalitis?

Answer 9

Viruses: enter virus, HSV1/2, VZ, arbovirus, adenovirus, HIV, M, R, rabies. Due to viral entry into blood and CNS. Leading to localized inflammation and parenchymal damage by inflammation.

Post measles: subacute sclerolising panencephalitis (SSPE). Due to immune mediated parenchymal reaction secondary to viral antigens, causing perivascular inflammation and demyelination.

Question 10

What is the epidemiology of encephalitis?

Answer 10

1/100k. Peak age 3-8 months.

Question 11

What may you find in the history of someone with encephalitis?

Answer 11

General: lethargy, irritable, poor feeding, hypotonia, behavioral change, vomiting,

Neuro: headache, confusion, photophobia, neck pain, seizures. FOCAL = HSV!

Question 12

What may you find in the examination of someone with encephalitis?

Answer 12

General: fever, low GCS, Kernigs sign + (pain on ext knee with hips and knees flexed in supine position)

Neuro: CN palsies, ATAXIA = VZV

Question 13

What investigations do you use for encephalitis?

Answer 13

Blood: FBc, blood culture, viral screen, UE, serum osm (SIADH RISK)

LP for CSF: WCC normal or high, protein may be mildly increased.

CSf microscopy, gram stain, sensitivity, HSV PCR, Serology for HSV Ab.

CT/MRI brian showing odema and focal lesions (mostly temporal in HSV).

ICP monitoring: may be required in extreme cases.

Question 14

What management do you do for encephalitis?

Answer 14

Empirical Abx should be commenced, 3rd gen cephalosporin (cefitraxone) until bacterial excluded.

Acyclovir then started IV if suspect encephalitis, followed by 3wk IV course if confirmed.

Support: fluid resusc, ICP monitoring, correct imbalance if SIADH, AED for seizures, analgesia for headache.

Regular neuro follow up after. Prevent with MMR vaccine.

Question 15

What are the complications of encephalitis?

Answer 15

HSV encephalitis may cause hemipareisis, deaf, epilepsy, bilateral motor changes, learning and language difficulties. Long term deficits may occur after arbovirus encephalitis and HIV too.

Question 16

What is the prognosis of encephalitis?

Answer 16

Many rake full recovery but dependent on stage when commencing Tx, aetiology and severity. 70% mortality rate with untreated HSVE.

Question 17

What is epilepsy and seizures?

Answer 17

Epilepsy is defined as >2 unprovoked seizures.

Seizure: paroxysmal synchronized cortical electrical discharges.

Question 18

What are the two types of seizures?

Answer 18

· Focal seizure: seizure linked to specific cortical regions (i.e. Frontal, temporal lobe etc). Subdivided into simple partial seizure (no LOC) and complex partial seizure (altered consciousness).

· Generalized seizure: seizure which affect consciousness. Can be tonic-clonic, tonic, myotonic, atonic, or absence.

Question 19

What are the types of primary epilepsy?

Answer 19

· Idiopathic generalized epilepsy

· Temporal lobe epilepsy

· Juvenile myoclonic epilepsy

Question 20

What are the reasons for secondary seizures?

Answer 20

· Tumors

· Infection (meningitis, encephaltitis, abscess)

· Inflammation (vasculitis and MS)

· Toxic/metabolic (glycaemia, hypocalcaemia, hyponatraemia, hypoxia, porphyria, liver failure)

· Drugs (withdrawal or use of alcohol or illicit drugs)

· Haem (stroke – haemoragic or infarction)

· Congenital: cortical dysplasia

· Malignant HTN or eclampsia

· Traum

Question 21

What does the common seizure mimic?

Answer 21

Common seizure mimics include syncope, migraine, or non-eplieptiform seizure disorder (dissociateive disorder)

Question 22

What is the most common cause of epilepsy?

Answer 22

Idiopathic

Question 23

What is the pathophysiology of epilepsy?

Answer 23

Seizures result form an alteration in balance of excitatory and inhibitory signals in the brain (due to altered currents – Na, K, or due to change in neurotransmitter activity (GABA, NMDA channels for glutamate). Precipitants include any trigger which increases impulse frequency and stimulation (flashing lights, drugs, stress, sleep deprivation, metabolic causes) but often are cryptogenic.

Question 24

What is the epidemiology of epilepsy?

Answer 24

1% prevalence in general population. Peak age of onset is childhood.

Question 25

What general symptoms of seizures may you get from a witness?

Answer 25

· Rapidity of onset · Duration of episode · Biting tongue/incontinence · Alteration in consciousness · Limb jerking · Post-ictal period of confusion · Drug history – alcohol and illicit drugs Parent too – child can be born with withdrawal.

Question 26

What may be associated with focal seizures in the history?

Answer 26

· Frontal lobe: motor convulsions. Jacksonian march (spreading clonus from lips or digits). Post ictal Todd’s paralysis (limb weakness, flaccid) · Temporal lobe seizures: Aura (visceral and psychic symptom of déjà vu) and hallucinaitons · Frontal lobe complex partial seizures: LOC with associated automatisms and rapid recovery · Partial seizures with 2 generalisation: focal followed by GTCS.

Question 27

What may be associated with generalised seizures in the history?

Answer 27

· Tonic clonic (GTCS): Vague symptoms before (irritability, tiredness) followed by attack. This consists of a tonic phase (extension of neck and head), and then clonic (repetitive muscle synchronous jerks) with fecal and urinary incontinence and tongue biting. After seizure there is lethargy, back pain, muscle stiffness, neck pain, headache, confusion. · Absence: usual onset in childhood 4-12. Pausing mid sentence with LOC but without loss of posture. Eyes may jerk or roll back, blinking or other repetitive actions like chewing. No postictal phase. Can occur 100x/d. · Non convulsive status epilepticus – acute confusional state, hard to distinguish from dementia · Myoclonic seizures: Sudden brief muscle contractions, cluster in a few minutes. May evolve into clonic seizure. · Status epilepticus: convulsions lasting >30min or repetitive convulsions >30 min with no regaining of consciousness in between.

Question 28

Describe the epilepsy syndromes

Answer 28

· Infantile spasms: 4-8m infants, cluster of myoclonic spasms, classic salaam attack where child jerks forward with arms flexed and hands extended. Chronic epilepsy and developmental delay. · Lennox Gastaut syndrome: Children aged 1-3y. Multiple seizure types (tonic facial, atonic, absence) developmental regression and LD. Chronic and resistant to therapy. · Benign childhood epilepsy with centrotemporal spike: 4-10y. Clonic seizures of face and upper limb in sleep, may progress to GTCS. AKA Rolandic epilepsy. Spontaneousy remit in adolescence. · Juvenile myoclonic epilepsy: adolescents, idiopathic generalized with myoclonic jerks, GTCS, and absence seizures on awakening. Require lifelong treatment but not associated with intellectual impairment.

Question 29

What may you find on examination of a patient with epilepsy?

Answer 29

Depends on aetiology – if primary, hard to se signs in inter ictal periods. Look for focal abnormality if secondary cause

Question 30

What investigations would you do for epilepsy?

Answer 30

Blood: FBC, UE, FLT, Ca, Mg, ABG, toxicology. PROLACTIN elevated transiently after true seizure. EEG: helps establish diagnosis and classification. Preformed interectally. Ictal EEGs very useful. CT/MRI: for secondary epilepsy. Rule out intracranial pathology. Other investigaitons: particularly for secondary seizures or if there si a suspected aetiology or suspect non neural cause of collapse. (ie LP, ECG, Echo, standing BP)

Question 31

How do you treat status epilepticus?

Answer 31

Status epilepticus (>30 min of continuous seizure or seizures without gain of consciousness in between) · Resuscitate and airway, breathing circulation! · Check glucose, hypoglycaemia? · IV lorazepam or PR diazepam -> wait 3 min, repeat if not better. X2. · If seizures recur, IV phenytoin under ECG monitoring. (or phenobarbitane, levitarecicam or sodium valproate) · If these fail, general anaesthesia with ventilation and intubation. Remember: · Treat cause: ie correct hypocalcaemia/glycaemia · Check plasma levels of anticonvulsants.

Question 32

What pharmacological agents can be used for seizure prevention in epilepsy?

Answer 32

Pharmacological prevention (if >2 seizures unprovoked). Start with 1AED · Lamotiragine(first line focal)/Carbamazepine (FOCAL) · Sodium valproate (GENERALISED) · Ethosuximide (ABSENCE) · Others: phenytoin, levetiracetam, gebepentin, vigabatin,

Question 33

What non medical management can be given for epilepsy?

Answer 33

Patient education: educate family on what to do, avoid triggers (ie alcohol and flashing lights), driving permitted if seizure free for 6m, supervise swimming. Drug interaction check (ie. OCP reduced effectiveness) AEDs reduce drug effectiveness as they are inducers of liver enzymes. ?Ketogenic diet may reduce seizure recurrence in AED resistant patients Surgery for refractive epilepsy: removal of identifiable epileptogenic focus (determined from EEG) or vagus nerve stimualtor.

Question 34

What are the complications of epilepsy?

Answer 34

Fractures in tonic clonic seizures, behavioral problems, sudden death in epilepsy SUDEP. Compications of AED – gingival hypertrophy, neutropenia, osteoporosis with CBZP, Steven Johnsons syndrome LMTG

Question 35

What is the prognosis of epilepsy?

Answer 35

50% remission 1y. 2/100k mortality py.