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Year 4 - PAN > Psychiatry - Neuropsychiatry > Flashcards

Psychiatry - Neuropsychiatry Flashcards

1
Q

What is the definition of epilepsy?

A

Discrete, recurrent abnormal electrical activity of the brain resulting in behavioural, sensory or motor changes, or changes in consciousness.

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2
Q

What is the aetiology of epilepsy?

A

Majority ideopathic. The aetiology of neuropsychiatric symptoms associated with epilepsy is a combination of biological and psychological factors.

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3
Q

How does epilepsy usually present?

A

Three stages:
1) Prodrome - irritability, tension, restlessness, insomnia; may occur hours or days before seizure

2) Ictal (during seizure) - symptoms depend on type of epilepsy; aura is only for localised seizures
- may experience acute perceptual changes, depersonalisation, acute mood changes, rising epigastric feelings

3) Post ictal (after seizure) - confusional state, may even experience transient paranoid hallucinations

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4
Q

What neuropsychiatric symptoms may occur in patients with epilepsy?

A

Personality changes
Psychosis - postictal, occurs after the seizure; interictal, occurs in between seizures and resembles schizophrenia
Depression
Aggressive behaviour

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5
Q

What investigations should be performed in cases of epilepsy?

A

Aimed at excluding other causes for seizures - e.g. post traumatic, cerebrovascular, SOL, drug/alcohol withdrawel, hypoglycaemia, hypoxia, encephalitis, syphilis, HIV

Diagnosis is usually on clinical grounds. EEG between episodes may be normal, but may help to localise the focus of the seizures. Serum prolactin levels are raised in the 15-20 minutes after a seizure.

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6
Q

How should epilepsy be managed?

A

1) Antiepileptic medication depending on the type of epilepsy; sodium valproate for generalised seizures, carbamazepine for partial seizures
2) Advise the patient not to drive and to inform the DVLA

3) For management of neuropsychiatric conditions, use psychotropics that do not lower seizure threshold
- treat depression with SSRIs
- treat psychosis with antipyschotics such as haloperidol, sulpiride or trifluoperazine

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7
Q

What is the psychiatric prognosis in epilepsy?

A

The major complication is suicide.

Mortality higher in patients with epilepsy than healthy controls.

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8
Q

What is non epileptic attack disorder?

A 
Dissociative seizures
Abnormal illness behaviour 
Difficult to distinguish from epilepsy
Usually have a past psychiatric history
Shorter post ictal confusion and unconsciousness 
Management is with CBT
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9
Q

What questions should be considered when ascertaining the risk of a head injury victim developing psychiatric symptoms?

A

Premorbid:

  • what was the patients ability to tolerate stress before the accident?
  • does the patient have any premorbid history of psychiatric disorders?

Trauma:

  • what part of the brain was injured?
  • how much of the brain was injured?

Convalescence:

  • are there any environmental or internal emotional stressors?
  • are there any ongoing medicolegal issues such as financial compensation?
  • has the patient developed epilepsy?
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10
Q

What psychiatric manifestations are common in head injury?

A

Cognitive impairment: may be progressive
Personality changes: impulsiveness, irritability
Post traumatic stress disorder
Depression
Post-concussion syndrome: headaches, dizziness, visual impairments, difficulty concentrating
Psychosis

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11
Q

How should psychiatric conditions arising in head injury be managed?

A

Depression: SSRI and TCAs
Psychosis: with atypical antipsychotics
Irritbaility/ agitation: carbamazepine, valproate
PTSD: psychological treatment, SSRI

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12
Q

What is Huntington’s disease?

A

Genetic illness characterised by choreiform involuntary movements and dementia.

Autosomal dominant disorder caused by multiple CAG repeats on chromosome 4p. This causes too few GABA-ergic and cholinergic neurones in the corpus striatum.

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13
Q

What are the risk factors associated with Huntington’s?

A 
Family history (or very occasionally a new mutation).
M=F
Usual onset 40-50 years.
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14
Q

What are the important clinical features of Huntington’s disease?

A 
Abnormal involuntary movements.
Psychiatric symptoms are common and include:
- dementia
- depression
- paranoia and psychosis
- behavioural change and irritability
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15
Q

What findings are present on an MSE in a patient with Huntington’s disease?

A

Appearance and behaviour - abnormal movements
Speech - normal
Mood - may be low or irritable
Perception - hallucinations in associated psychosis
Thoughts - normal or paranoid ideation
Insight - insight may be good preceding dementia
Cognition - impaired in dementia

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16
Q

What investigations are performed in Huntington’s disease?

A

Genetic testing.

Children of an affected parent have a 50% chance of inheriting the condition.

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17
Q

What is the prognosis of Huntington’s disease?

A

Management is symptomatic.
The main complication is suicide risk for patients and their relatives.
Huntington’s is more severe the earlier the onset and the average duration of the illness is 11-20 years. The chorea is followed eventually by dementia, seizures and death. No treatment can prevent progression.

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18
Q

What is motor neurone disease?

A

Lower and upper motor neurone degeneration without sensory symptoms. Unknown aetiology.

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19
Q

What risk factors are associated with MND?

A

Unknown, but many factors including viruses (polio) and genetics (chromosome 21) have been considered.

Onset age is between 50-70 years, more common in males.

20
Q

What is the history of MND?

A

Stumbling, spastic gait, foot drop
No sensory symptoms
Sleep disturbance, fatigue
Psychiatric manifestations: depression, emotional lability (pseudobulbar palsy)

21
Q

What are the examination findings associated with MND?

A

Upper and lower motor neurone signs on examination
No sensory impairment
MSE:
- Appearance - may be fatigued, depressed
- Speech - normal, depending on cranial nerves being intact
- Emotion - emotional lability
- Perception - normal
- Thoughts - normal
- Insight - good
- Cognition - mild cognitive deficits may rarely progress to dementia

22
Q

How is MND investigated and managed?

A

MRI, LP to exclude structural/ inflammatory causes.

Treat symptoms - e.g. baclofen for spasticity
Treat depression with antidepressants
Pain control with opioids may be needed

23
Q

What is the prognosis of MND?

A

Frontal lobe dementia (very rare) can be a complication.

MND is a progressive disease and most die within 5 years of diagnosis.

24
Q

What is multiple sclerosis?

A

Disease characterised by multiple plaques of demyelination and axon loss throughout the CNS (predominantly white matter). The aetiology is unknown.

25
Q

What is the epidemiology of MS?

A

More common in the western world and in areas with temperate climates.
F>M
20-40 years peak age of onset

26
Q

What is the history of MS?

A

Physical:

  • fatigue
  • spasticity
  • motor weakness
  • numbness
  • bladder spasticity
  • swallowing problems
  • visual disturbances (optic neuritis)
  • ataxia

Psychiatric:

  • transient mood changes
  • suicidal ideation
  • depression
  • euphoria
  • psychosis hysteria and hypomnia (rare)
27
Q

What are the important findings on an MSE in a patient with MS?

A 
Appearance - may be anxious, irritable 
Speech - normal
Mood - low or may be euphoric 
Perception - none 
Thought - usually normal
Insight - good
Cognition - impaired memory, attention, abstract thinking
28
Q

What investigations should be undertaken in MS?

A

MRI shows plaques of demyelination. CSF shows oligoclonal IgG bands on electrophoresis.

29
Q

How is MS managed?

A 
Beta interferon: reduces frequency of relapses 
Methylprednisolone 
Baclofen (for muscle spasms)
Antidepressants 
Low dose antipsychotics
30
Q

What is the prognosis in MS?

A

Psychosis is rare, epilepsy can occur as a complication.

MS is a progressive disease. Prognosis is worse if older, male or has many early relapses/ early disability.

31
Q

What is the underlying pathology in Parkinson’s disease?

A

Parkinson’s disease is reduced dopaminergic activity in the striatum causing movement disorders: tremor, rigidity, bradykinesia and difficulty starting and stopping walking. The underlying aetiology is degeneration of dopaminergic neurones in the substantia nigra pars compacta.

32
Q

What are the risk factors associated with Parkinson’s disease?

A

Mitochondrial mutations resulting in reduced ATP.
Pesticides and toxins have also been implicated as possible causes.
Neuroleptics and Wilson’s disease may cause a similar Parkinsonian syndrome.

33
Q

What are the symptoms of PD? What psychiatric symptoms are most common?

A

Resting tremor, rigidity, slow movement, monotonous steps (festinant gait)

Psychiatric symptoms are common, esp:

  • depressive symptoms (reactive to neurotransmitter abnormality) 70%
  • cognitive deficits in 10-20%
  • psychoses (due to long term treatment) paranoid delusions or visual hallucinations
34
Q

MSE in PD

A

Appearance and behaviour: mask like face, reduced facial expression, tremor
Speech: slow, monotonous
Emotion: depressed
Perceptions: rarely may have abnormal perceptions (visual hallucinations)
Thought: rarely have psychotic symptoms - e.g. paranoid delusions
Insight: variable
Cognition: 10-20% have cognitive defects

35
Q

Management of psychiatric symptoms in PD

A

Use atypical antipsychotics for psychosis - less likely to induce extrapyramidal side effects

Treat depression with nortriptyline

Acetylcholine esterase inhibitors (rivastigmine) - may benefit cognition and hallucinations

36
Q

Organism that causes syphilis

A

Infection with Traponema pallidum (spirochete infection)

Usually sexually transmitted

37
Q

What are the four clinical stages of syphilis infection?

A

Need to know sexual history, contacts also at risk

Primary - localised lesion; infected painless hard ulcer at the site of infection (chancre)
Secondary - 1-2 months later. More generalised lesions and fever, lymphadenopathy and rashes
Tertiary - rare. 6 years after primary infection. Granulomas (gummatous lesions) occur in the skin and mucosa
Quarternary - 8-12 years after primary infection. Affects brain and spinal cord and may lead to meningovascular effects, such as delirium and dementia. May progress to tabes dorsalis and/or general paresis of the insane (GPI)

38
Q

Tabes dorsalis

A 
Feature of quarternary syphilis 
Occurs in approximately 20% of cases of GPI 
Lightning pain, especially in the legs
Sensory ataxia
Gait disturbances 
Numbness
39
Q

What is general paresis of the insane?

A

Occurs approximately 20 years after initial infection but this may vary
Personality changes and irritability
Dementia
Depressive symptoms
Grandiose delusions/ expansive ideas about wealth, power or sexual prowess
Rarely can lead to full blown schizophreniform illness

40
Q

Examination findings in syphilis

A

Tremor
Dysarthria
Increased muscle tone and reflexes (hypereflexia)
Inco-ordination
Argyll-Robertson pupil: small, irregular pupil with normal reaction to convergence (accommodation) but not reaction to light. Seen in meningovascular syphilis

41
Q

Management of syphilis

A

Procaine penicillin (daily IM injections) - may induce neuropsychiatric improvement even in severe disease

42
Q

What is Wilson’s disease?

A

Hepatolenticular degeneration due to copper deposits in various sites throughout the body, esp lentiform nucleus and liver.
Autosomal recessive, chromosome 13.

43
Q

History of Wilson’s disease

A

Copper can be deposited in the:

  • cerebrum –> dementia
  • basal ganglia –> tremor, akinetic rigid syndrome, choreo-athetosis
  • liver –> cirrhosis, jaundice, hepatosplenomegaly
  • eyes –> Kayser-Fleischer rings
  • bones –> osteoporosis, osteoarthritis
  • kidneys –> renal impairment
44
Q

How common are psychiatric symptoms in Wilson’s disease?

A

Up to 60% of patients with Wilson’s have psychiatric symptoms:

  • behavioural and personality changes
  • depression
  • irritability
  • psychosis
  • cognitive changes in dementia
45
Q

Investigations in Wilson’s disease

A

Serum copper is low
Caeruloplasmin low
Hypodensities in basal ganglia seen on CT

46
Q

How is Wilson’s disease treated?

A

Mainstay of treatment is reduction of copper levels using dietary copper restriction and/ or chelating agents such as D-penicillamine

Year 4 - PAN (43 decks)

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