Extrapyramidal Paralysis and Tone Alteration
The pathogenetic basis of extrapyramidal paralysis (or paresis) is damage to the neurons of the extrapyramidal system. This results in a specific complex of motor disturbances that primarily affects the patient's tone and posture.
Key clinical manifestations include:
- Increase in muscle tone of the rigid type. Tone increases uniformly across virtually all muscle groups: flexors and extensors, pronators and supinators are equally tense.
- Muscle rigidity. A classic rigid paralysis is formed.
- Catalepsy. The term originates from the Ancient Greek κατάληψις (seizing, holding). This is a condition in which the patient's body or limb freezes for a prolonged period in any position artificially imparted to it. Catalepsy is always combined with slowed movement and impaired coordination.
- Posturotonic (postural) reflexes. These occur when the body's position in space changes. A characteristic example is the appearance of nystagmus of the eyes or head when the patient's body is rotated.
Important differential sign: extrapyramidal lesions lack pathological reflexes and do not show pronounced hyperreflexia. This is a critical criterion for distinguishing this pathology from central (pyramidal) paralyses.
Hyperkinesia, Spasms, and Tics
Hyperkinesia (from Ancient Greek ὑπέρ — over, extreme, and κίνησις — movement) represents a prototypical form of neurogenic disorder. It is expressed as excessive, violent movements arising from impaired regulation of motor acts. Both the amplitude and frequency of involuntary movements increase.
The pathogenesis is based on lesions of various structures of the extrapyramidal system, which normally ensures the control of movements, muscle tone, and posture (outside the responsibility of the pyramidal tract). Athetosis and spasmodic torticollis also belong to this group of extrapyramidal disorders.
The causes of hyperkinesia are diverse and include both organic and functional disorders:
- Neurodegenerative diseases (e.g., hereditary autosomal dominant Huntington's disease).
- Multiple sclerosis and encephalitis.
- Intoxications, including side effects of neuroleptic medications.
- Brain tumors and traumatic brain injuries.
- Cerebrovascular disorders.
- Cerebral palsy.
Spasms are classified separately as a typical form of movement pathology. These are suddenly occurring involuntary paroxysmal or continuous muscle contractions that vary in intensity, duration, and distribution.
Tics also develop when the extrapyramidal system is damaged. The most frequent etiological factors for tics include stress, psychological trauma, hypovitaminosis, as well as organic brain damage (trauma, encephalitis), vascular disorders, and intoxications (including antipsychotics and neuroleptics).
Myasthenic Hypokinesia
Myasthenic (synonyms: neuromuscular, synaptic) hypokinesia unites a group of pathologies, the most famous of which is myasthenia gravis (myasthenia gravis), alongside other myasthenic syndromes.
The pathogenetic basis of the disease is impaired excitation transmission at cholinergic neuromuscular synapses (at the stage of signal transition from motor axon terminals to skeletal muscle fibers). Transmission is disrupted due to problems involving acetylcholine.
Two main developmental mechanisms are distinguished:
- Blockade of postsynaptic cholinergic receptors by specific antibodies (Ig). Immunoglobulins tightly fix to the postsynaptic membrane of the muscle fiber and physically prevent acetylcholine molecules from interacting with the cholinergic receptor.
- Decreased muscle fiber response to acetylcholine. This may be caused by hyposensitization of cholinergic receptors to the neurotransmitter or the dominance of low-affinity cholinergic receptors on the muscle fibers.
Clinically, myasthenic hypokinesia manifests as muscle weakness of varying severity and extremely rapid muscle fatigue during physical exertion.
Ataxia as a Coordination Disorder
Ataxia (from Greek ataxia — disorder, lack of coordination) is a prototypical locomotor disorder characterized by impaired spatial and temporal coordination of voluntary movements. It is strictly unrelated to impaired muscle strength (it is not accompanied by paresis or paralysis).
A whole complex of neural structures is responsible for coordination in the body: the cerebellum, spinal cord, frontal and temporal lobes of the cerebral cortex, midbrain, thalamus, and labyrinth.
Depending on the localization of the pathological process, the following forms of ataxia are distinguished:
- Cerebellar ataxia — develops with direct damage to cerebellar structures.
- Cortical ataxia — occurs in pathology of the frontal and temporal areas of the cerebral cortex.
- Vestibular ataxia — associated with damage to the vestibular apparatus.
- Psychogenic ataxia — a specific form observed in severe distress syndrome.
A special place is occupied by sensory ataxia. Its pathogenetic basis is damage to the proprioceptive sensory pathways, causing the brain to stop receiving correct information about the body's position in space.