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Neuroscience BB Exam 3 > Disorders of CNS > Flashcards

Disorders of CNS Flashcards

1
Q

What is a generalized epileptic seizure? Status epilepticus? Grand mal?

A

Affects BOTH sides of the brain

  • MOST DANGEROUS form with tonic-clonic seizure lasting 30min+ without recovery of consciousness between attacks
  • synchronous activation of large populations of neurons –> universal motor manifestations
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2
Q

What are partial epileptic seizures?

A

Focal, affecting ONLY small regions

- Focal nature results in focal impairment (i.e. small motor manifestations)

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3
Q

What is Rasmussen’s Encephalitis?

A

Overactivity of glutamate pathway due to developed excitatory antibodies that bind glutamate receptors (AGONISTS)
- trauma allows for the antibodies to cross the blood brain barrier; seizure then causes more BBB leak and more antibody crosses, etc.

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4
Q

Consequences of Rasmussen’s Encephalitis?

A

Cerebral damage, lactic acidosis, hypoglycemia, hyperpyrexia

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5
Q

What is the main reason for epileptogenesis in the limbic structures (hippocampus)?

A

The rhythmic bursting activity of that region

  • GABA/Glutamate balance is KEY because imbalance between excitation/inhibition is classic sign of epileptic seizure
  • Hippocampal and limbic region show a lack of GABA
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6
Q

Diagnosis of epilepsy?

A

EEG or MRI!

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7
Q

List some general treatments of epilepsy.

A
  • Medication - Antiepileptic drugs (AEDs)
  • Surgery
  • Vagus nerve stimulation (those not surgical candidates and pharmacological resistance, low success rate)
  • Ketogenic diet (2 out of 3 may prevent seizure, 1 out of 3 prevent completely, mechanism unclear (switch from glucose to ketone bodies))
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8
Q

List some classes of AEDs:

A
  • Sodium channel blockers - prevent repetitive axon firing
  • T-type Calcium channel blockers - inhibit rhythmic thalamocortical spike/waves bursts
  • AED’s acting on GABA - agonists, reuptake inhibitors, GAD enhancers (enhance synthesis), inhibiting GABA-transaminase
  • Glutamate blocker - (AMPA, NMDA, glycine, metabotropic)
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9
Q

When/how is epileptic surgery done?

A
  • Used when epilepsy is pharmacologically resistant, most commonly in the form of temporal lobe resection, rates of success are 30-80%
  • MRI, PET, single-photon emission CT (SPECT) of ictal-interictal cerebral blood flow –> Identify epileptic focus
  • Magneto-encephalography with fMRI, EEG can map location of interictal epileptic dischargers
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10
Q

List some anxiety disorders (7):

A
  • Generalized Anxiety Disorder (GAD)
  • Phobia
  • OCD
  • Acute stress disorder
  • PTSD
  • Agoraphobia
  • Panic disorder
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11
Q

What is GAD?

A

Causes motor (trembling, twitching), autonomic (shortness of breath, palpitations), psychological symptoms

MAIN SX: unrealistic or excessive worry for 6mo+

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12
Q

What are some theories for causes of GAD?

A
  • Deficiency in GABA within the amygdala strongly implicated, other substances also involved
  • Hypothesis that uncoupling of anterior cingulate-amygdala circuit occurs
  • Genetic link between short allele for 5’ promoter of serotonin uptake leads to increased anxiety
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13
Q

Treatment for GAD?

A
  • Benzodiazepines (Valium) – GABA agonist (depressing neurons within the amygdala)
  • Enhancing serotonin – via SSRIs and MAOI’s as well as buspirone
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14
Q

What is Major Depressive Disorder?

A

One or more major depressive episodes lasting 2wk+, seen in unipolar and bipolar depression

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15
Q

What is Unipolar Depression?

A

Occurs 2-3x more women, average onset at 30yo

Endogenous depression with no precipitating cause (40-60% of those hospitalized for depression) as opposed to reactive depression (from loss of loved one)

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16
Q

Describe a proposed mechanism for depression.

A

In severe depression, hypersecretion of CRH –> increased ACTH –> increased cortisol; NE can stimulate CRH release

Suggestion that hypercortisolemia damage to hippocampus mood changes

17
Q

Treatment for unipolar depression?

A
  • SSRIs
  • Serotonin and NE reuptake inhibitors (SNRIs)
  • NE and dopamine reuptake inhibitors (NDRIs)
  • Tricyclic antidepressants
  • MAOI
18
Q

What is Bipolar Disorder (Manic-Depressive Illness)?

A

Distinguished from Unipolar Depression based on depression with punctuated episodes of elevated, expansive, irritable mood
- Thinking is fluid, speech and physical activity excessive, inflated self-image (MANIA) occurring every 2-4yr but can occur annually or more frequently

Possible link to inositol-1-phosphatase overactivity in neurons of those with manic depressive illness

19
Q

Treatment for Bipolar Disorder?

A
  • Lithium carbonate – block inositol-1-phosphatase from the PIP2 second messenger system, blocking results in buildup of IP3 and subsequent reduced neuron response to those neurotransmitters associated with this cascade
  • Antidepressants – used during the depressive phase
20
Q

Positive symptoms of schizophrenia?

A

Delusions, hallucinations (visual/auditory), disorganized speech or thought, purposeless behavior

21
Q

Negative symptoms of schizophrenia?

A

Reduced range and intensity of emotional expression, lessening speech fluency/productivity, laconic, empty replies, inability to initiate/persist in goal-directed behavior

22
Q

Who is affected by schizophrenia?

A
  • Affects 0.5-1% of the population, leading to social withdrawal (homelessness), however the threshold for schizophrenia is not very precise
  • SX show in 20s earlier in men (18-25), 1/5 recover, 1/10 commit suicide
23
Q

What is the Diathesis-stress model?

A

Strong genetic component which conveys a genetic vulnerability, which in combination with an environmental or psychosocial stressor, causes the disease

24
Q

Some proposals for cause of schizophrenia:

A
  • PFC volume reduced from DECREASED SYNAPTIC CONNECTIVITY (not from loss of neurons), which causes a disorder of working memory (attention) –> inattention, poor associations, etc.
  • Altered activation of dopamine receptors diminished cortical dopamine function (NOT the whole answer)
25
Q

Things that cause schizophrenia-like symptoms?

A
  • PCP causes schizophrenia like symptoms coupled with dopamine hypofunction
  • Seen in NMDA receptor blockers (phencyclidine/ketamine)
26
Q

Limitations of drugs in treating schizophrenia?

A

Drugs not useful to help cognitive impairment; treat the positive symptoms BUT NOT THE NEGATIVE SX (lack of motivation, emotion prevent normal social relationships)

27
Q

Drugs used to treat schizophrenia (the positive symptoms):

A

Antipsychotics block D2 receptors
- Also acts on the basal ganglia –> tardive dyskinesia, rigidity, akinesia (extrapyramidal side effects)

Clozapine – “atypical drug” high affinity for D4 dopamine receptors and low affinity for D2 receptors prevents some of the extrapyramidal side effects; however other actions probably exist for this drug

28
Q

Characteristics of Alzheimer’s:

A

Symptoms onset after age 60 but early onset forms exist; symptoms are decline in thinking ability, memory, movement, language, judgment, behavior, abstract thinking, nearly all brain functions are eventually affected

Typical cause of death is pneumonia (aspiration)

  • Suggested cause is gene for amyloid beta-protein precursor (betaAPP)
29
Q

Anatomy particularly affected:

Anatomy particularly spared:

A
  • Association cortex, nucleus basalis of Meynert and hippocampus/parahippocampal structures, locus ceruleus, & dorsal tegmental nuclei –> narrow gyri and widened sulci
  • Primary somatosensory/visual/auditory cortex, motor cortex, cerebellum, basal ganglia, brain stem, thalamus
30
Q

3 categories of Alzheimer’s:

A
  • Early onset familial (65yr)

- Sporadic late onset (>65yr) = 75% (leading cause of dementia and death in those over 65yr)

31
Q

Some histological characteristics of Alzheimer’s:

A
  • Neurofibrillary tangles (composed of hyperphosphorylated Tau protein)
  • Neuritic plaques (composed of amyloid beta-protein)
32
Q

Amyloid beta protein has three enzymes (secretases) for processing (therapeutic targets) – What are they?

ABP is glycosylated transmembrane protein – processing important for the formation of the plaques

A
  • Beta-secretase – amyloidogenic pathway IN COMBINATION with gamma-secretase
  • Gamma-secretase – intramembrane protease, amyloidogenic IN COMBINATION with beta-secretase
  • Alpha-secretase – amyloid beta fragment forming (non-amyloidogenic) = SOLUBLE
33
Q

How are amyloid plaques formed?

A

Amyloidogenic secretases form an amyoid beta-protein oligomer –> polymerize to INSOLUBLE amyloid –> INFLAMMATORY RESPONSE

34
Q

How are neurofibrillary tangles formed?

A

Tau protein is hyperphosphorylated from activation of kinases

35
Q

Treatments for Alzheimer’s?

A
  • Anticholinesterase drugs – modest improvement from initial loss of nucleus baslis of Meynert for improving cognition; ONLY effective for 6-12 months
  • Drugs acting on glutamate – Memantine – NMDA antagonist –> reduce excitotoxic effects showing slowing of the declined behavioral and intellectual functioning but doesn’t modify pathology
36
Q

Future approaches to treatment of Alzheimer’s?

A
  • Vaccine to Amyloid beta
  • Antibodies to A-beta
  • Brain cell apoptosis inhibitor
  • Neuroprotection
  • Fibrilization of amyloid-beta prevention

Neuroscience BB Exam 3 (9 decks)

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