Lecture 7 - Encephalitis Flashcards
(Encephalitis) When a disease process invades the CNS via bloodstream nose or peripheral nervous system it can result in what types of encephalitis?
- Infectious encephalitis (e.g., HSV)
- Post infectious encephalomyelitis (e.g., ADEM)
- Slow viral CNS infection (e.g., HIV, SSPE)
- Autoimmune (e.g., Rasmussen’s, anti NMDA-receptor antibody, Cerebral Lupus)
Describe the features of Herpes Simplex Encephalitis.
HSV type; pathophysiology/brain areas affected; treatment, prognosis
About a third of HSV encephalitis occurs in children, majority is HSV 1 type.
NEUROPATHOLOGY:
- Neuropathology is often bilateral (if uni-lateral, typically more left-sided)
- In CHILDREN: Inflammation typically affects temporal-limbic structures, occasionally orbitofrontal (severe cases).
- In NEONATES: generalised brain damage (incl. hippocampal).
Treated with acyclovir
Usually poor outcome, only 13% full recovery
Describe the cognitive outcomes associated with Herpes Simplex Encephalitis.
Cognitive outcome:
- variable
- mild memory disorder to amnesia (full)
- problems with emotional control & anxiety (can be 2nd to awareness of cognitive changes post-illness)
- Cognitive fatigue
CASE: (THINK ABOUT IF and how this is CONISTENT WITH HSV encephalitis)
age 5 diagnosed with HSV
premorbid history of typical development
initially, global cognitive deficits
significant attention deficits & hyperactive behaviours developed as a result of the HSV and persisted.
Significant hearing loss
6 months post - global cognitive deficits (verbal and visual memory, executive dysfunction, verbal comprehension, perceptual reasoning, processing speed)
5 years post - improved VC, PR, Coding, verbal learning, Visual memory, story memory (improving). + left with self-regulatory & attention, distractible/impulsive (diagnosed with secondary ADHD).
Yes.
Initially wide-spread cognitive deficits. 6 months post resolution, deficits of medio-temporal origin (e.g., memory) improving, as is IQ and processing speed. However, fronto-exec deficits remain.
ADHD secondary to encephalitis.
Describe the features of HIV in children.
epidemiology; aetiology in children; disease process; mortality
Not particularly common in Australia, 80-100 known children (23 in NSW).
Transmits to children via ‘vertical transmission’ (in-utero, during labour or via breastfeeding); very rarely through blood transfusions (better monitoring!).
CD4 cells (type of protein) - white blood cells on surface of T-cells and other immune cells. HIV attaches to the CD4 cells allowing the virus to enter and infect the CD4 cells, damaging them in the process. FEWER functioning CD4 cells = more vulnerable to infection/illness (CD4 15-25% = moderate immunosuppression; CD4
When does HIV become AIDS?
HIV = the virus, which can lead to AIDS.
Viral load (measured with blood test) and CD4 count are considered together to determine the staging and outlook of the disease.
CD4 cell count
What are the classes of HIV disease progression in children?
N = not symptomatic A = mildly symptomatic B = moderately symptomatic C = Severely symptomatic = hx of AIDS defining illness, HIV related progressive encephalopathy (NCD HAND), Primary lymphoma in brain, brain toxoplasmosis
Describe HAART for HIV
Highly Active Anti Retroviral Treatment. Is a combination of 3 or more different states by inhibiting the enzymes that the virus uses to multiply - this slows (near halt, but not quite) the HIV process.
Resistance is a major issue (virus can become resistant quickly). Long term toxicity issues increasingly identified (particularly high dose regimes).
No neuropsychological side effects identified in children. ? relationship b/w cognitive functioning & use of HAART.
How does HIV lead to CNS disease processes?
HIV associated with increased risk for central nervous system because the virus can permeate the blood-brain barrier.
Infects macrophages and microglial cells (main target), resulting in immune dysregulation, production & release of cytotoxic molecules. Interaction with astrocytes may accelerate neurotoxic mechanisms.
Can result in:
- Cerebral atrophy
- Ventricular enlargement
- Demyelination
- Calcifications, most evident in basal ganglia, cerebellum, subcortical frontal white matter
What are the four broad patterns/courses that HIV encephalopathy can take in terms of children’s cognitive development?
- Subacute progressive: gradual loss of previously obtained milestones, progressive bilateral pyramidal tract signs
- Plateau: variable periods of time in which little or no cognitive dev occurs, failure to attain new milestones until ultimate regression
- Static: steady acquisition of cognitive and motor skills, although not at a normal rate
- mild cognitive impairment
What factors contribute to cognitive outcomes in children?
HIV has subtle effects on cognition, but family and illness/enviro also contribute.
Illness effects:
- direct virus effects on CNS
- ? introduction of HAART medication regime
- long periods of absence from school due to illness
- Low birth weight and/or prematurity
- Medication adherence, 90% required
Family factors
- genetics, hx of learning difficulties, ADHD etc
- parent psychopathology and/or substance use
- parent death or illness
- foster care placement
Environmental stressor
- SES and associated opportunities
- school absent
- Stigma, isolation
What are the social/emotional outcomes associated with HIV, are they a direct cause of the disease?
Behaviour problems, anxiety, depression, suicidal ideation/suicide attempts, stigma related issues (E.g., school disclosure, acceptance of interventions, medication adherence).
Primarily due to enviro/family stressors.
Describe Rasmussens ….
Rare degenerative form of epileptic encephalopathy
inflammatory process- usually affects one hemisphere
-Typically occurs age
What is the treatment for Rasmussens? What is the cognitive outcome after surgery?
Treatment - hemispherectomy to control seizures, halt mental deterioration and stop progression to other hemisphere (corpus callostomy not as effective). (seizures so frequent and severe, don’t respond to treatment).
cognitive outcome after surgery:
- preexisting hemiparesis so risk of additional motor deficits low
- modest developmental gains post-surgery, often limited by severe pre-existing damage in non-operated hemisphrere
- Most consistent predictor: shorter duration of epilepsy preceding surgery
- Age at onset of Sz, freq, and severity of Sz
- Most studies report little change to cognitive function post-surgery – damage already one.
