I. Answers A, B, C and E are true statements, whereas D is not.
II Answers A, D and E are true statements, whereas B and C are not.
III. Answers A, C, D and E are true, whereas B is false.
1. Degeneration of dopaminergic neurons in the substantia nigra results in severe lack of dopamine in the striatum. Lack of dopamine overactivates the GABA pathways to the motor thalamus, which activates the motor cortex neurons. The descending motor command probably increases the discharge of both alpha- and gamma- motor neurons in the spinal cord.
2. Parkinson’s disease.
3. The GABA pathways overactivate thalamus due to the lack of dopamine in the striatum. Hereby, the motor cortex neurons are activated, and they increase the discharge of static gamma- motor neurons in the spinal cord.
1. The event started as a partial or focal seizure, with the focus in the face and hand area of the right motor cortex. Then the overactivity spread to become generalized - a so-called grand mal seizure. The spread in a particular pattern is called Jacksonian march.
2. The EEG probably shows high-voltage-high-frequency discharge over the entire cortex during the grand mal seizure. Following the seizure the EEG is possibly normal, as many epileptic patients have normal EEG activity between attacks.
3. Tonic convulsions of the entire body and loss of consciousness characterise general epileptic seizures (eg. grand mal). Most of the brain is involved in a neuronal circuit activation. The hyperactive nerve cells release K+ and glutamate/aspartate. Epileptic seizures are either initiated or propagated through NMDA-receptors on the neurons. NMDA-receptors contain ion channels that are also voltage-gated. NMDA-receptors are also called excitatory amino acid receptors (EAA-receptors), because both amino acids are excitatory. Lack of inhibitory neurotransmitters, such as GABA, may also be involved in the neuronal overactivity.
4. The blood glucose was normal (5 mM), so hypoglycaemia was excluded.
1. Alzheimers disease is a form of presenile dementia (occurring before the age of 70), where the loss of mental powers is rapid. - Simple dementia is insidious but also caused by cortical atrophia.
2. The age of the patient is compatible with presenile dementia, and the rapid loss of mental powers in a case of cortical atrophia is characteristic of Alzheimer’s disease.
3. The prognosis is poor for both disorders, and the Alzheimer patient may die within a few years of opportunistic infections.
4. Most cases of Alzheimer’s disease occur sporadically, but Alzheimer families exist. The gene defect causing familial Alzheimer disease is located on chromosome 21, close to the pro-A4 gene.
5. At autopsy argentophilic plaques filled with amyloid protein A4 are found in the hippocampus, basal ganglia, thalamus and the cortex. The weight of the brain is 925 g.