89. General regularities in occurrence and development cns disorders. Pathological processes classification.

Classification:

I. By anatomical principle:

1) peripheral nervous system disorders;

2) central nervous system disturbances:

1. spine;

2. medulla oblongata;

3. midbrain;

4. cerebellum;

5. intermediate brain;

6. basal ganglia (strio-pallidar system);

7. forebrain (hemispheres).

II. By origin:

1) hereditary;

2) acquired:

a) primary – while pathogens direct action to CNS; factors groups: physical (trauma, radiation, thermal influencings), chemical (toxins, poisons), biological (viruses, bacteria), social (word);

b) secondary – are determined by homeostasis disturbances (hypoxy, hypoglycemy, acidosis), immune factors (autoallergic reactions), brain circulation disturbances.

III. Cellular principle:

1. electrophysiological processes disorders;

2. neuro-chemical (mediator) processes disturbances;

3. axoplasmatic transport disorders.

IV. Dependently on injured functions type:

1. sensoric functions (sensitivity) disorders:

   1. hyperesthesia;

   2. hypesthesia;

   3. anesthesia.

2. effector functions disorders:

   1. motor;

   2. trophyc;

   3. vegetative.

3) integrative functions disorders.

90. Pathological excitement and inhibiting in nervous centers.

I. Of pathological excitement:

1. ionic disorders: K-ions extracellular level increasing and Ca extracellular content diminishing;

2. ephaptic effects;

3. exciting neurotransmitters concentration increasing in synaptic cleft;

4. agonists action to exciting post-synaptic receptors;

5. inhibitory mediators level diminishing in synaptic cleft;

6. blockade of postsynaptic reeptors percepting inhibitory mediators.

II. Of pathological inhibiting:

1. ionic disorders: K-ions extracellular level decreasing and Ca extracellular content increasing;

2. electrogenic ionic pumps and their energetic consumption disturbances;

3. excitory mediators level diminishing in synaptic cleft;

4. blockade of postsynaptic reeptors percepting excitory mediators;

5. inhibitory neurotransmitters concentration increasing in synaptic cleft;

6. agonists action to inhibitory post-synaptic receptors.

Pathological excitement and inhibiting results in CNS:

1. Excitement summation.

2. Excitement rhythm transformation.

3. Nervous centers fatigueability increasing (they belong to the most fatigueable structures in CNS).

4. Excitement durable afteraction – excitement reverberation.

5. Pathological dominanta.

91. Ephaptic effects.

Ephapses are electrical synapses. In ephapse electrical current sourse is presynaptic cell membrane. Only depolarization process is possibl (so, electrical synapses can be only excitory ones), impulses can distribute in 2 directions, velocity of such transmittance is bigger than in chemical synapses (because synaptic cleft is lss). There are connexones (6 globular proteins complexes). CNS, myocardium and smooth musculature are rich in ephapses. Due to this fact, one can tell about functional syncitium through which impulses can come very quickly, without excessive energy loosing. All embryonic connective and epithelial tissues are rich in such electrical synapses.

Axones can be injured at some disease. As it is known, one of the most important laws of nervous transmittance is law of isolated conductance transmittance. At axon cutting both proximal and distal part of it is degenerated. It will regenerate in some months in peryphral nervous system but its growing de novo processuses are demyelinized first. Myeline membrane injury will lead to mentioned law disorders. Besides, there can b axonic neuropathies the main symptom of which is axonic transport disturbance.

Demyelinized axons the mostly often participate in abnormal interactions. Impulses oming through groups of nervous fibers induce excitement of other parallel axons. It is known as ephaptic transmittance. When such anomalous action potentials are generatd in sensoric nervous fibers the patient has anomalous sensations as paresthesias. They can be agonizing, especially when they are connected with noceoceptive fibers. Neuralgias, kauzalgias (burning and dumning without distinct location), neuromic pains can be present. Interaxonic disorders can be the result not only of insufficient isolation (with myelinic membranes) but also increased axonic excitability.

These mechanisms, excitement reverberation and pathological dominanta are on the base of epilepsy.