Classification of Motor Disorders
Depending on which structures of the nervous system are affected, four main types of paralysis and paresis are distinguished:
- Central (also known as pyramidal or spastic);
- Peripheral (lower motor neuron);
- Extrapyramidal;
- Myasthenic (associated with impaired neuromuscular transmission).
Clinical Manifestations of Central Paralysis
The pathogenetic basis of spastic paresis is damage to the pyramidal system. Due to the weakening of inhibitory descending influences from the brain, the segmental apparatus of the spinal cord becomes disinhibited. This forms a classic symptom complex:
- Hyperreflexia. Manifested by an increase in segmental tendon and periosteal reflexes. The amplitude of the reflex response significantly increases, and reflexogenic zones expand.
- Spastic Muscle Hypertonia. Muscle tone in central paralysis increases unevenly. A typical distribution is formed: in the upper limb, spasticity predominates in the shoulder adductors and forearm flexors; in the lower limb, the hip and knee extensors, hip adductors, and ankle plantarflexors are tense. Over time, such persistent limitation of movement leads to the fixation of the limb in an unusual position, resulting in neurogenic contractures.
- Pathological Reflexes. Subdivided into flexor and extensor types (e.g., Babinski, Rossolimo, Bekhterev reflexes). Extensor reflexes serve as one of the earliest and most constant signs of pyramidal tract lesions.
- Clonus. Represents an extreme, high degree of tendon-muscle reflex hyper-reactivity. Clinically, it appears as a series of rapid rhythmic muscle contractions (spontaneous or in response to a stimulus). Most commonly observed as ankle, patellar, wrist, or clonus of the jaw.
- Syncinesias. These are involuntary associated movements. They occur in the paralyzed limb when the patient performs a voluntary movement with the healthy limb or another part of the body, mediated by the spinal cord, cerebellum, and pyramidal system.
Extrapyramidal Disorders (Rigidity)
When the extrapyramidal system is damaged (as seen, for example, in parkinsonism), a different type of tone alteration develops—rigid paresis. Its pathogenetic mechanism involves the simultaneous increase in tone of both flexors and extensors.
Clinically, this is manifested by the phenomenon of "lead-pipe" or "cogwheel" rigidity: the patient's trunk or limb is able to maintain an externally imposed posture for a long time.
Peripheral (Flaccid) Paralysis
The pathogenetic basis of peripheral paralysis consists of primary (hereditary, congenital) or acquired lesions of the peripheral motor neurons (anterior horn cells of the spinal cord, cranial nerve nuclei).
Acquired damage develops under the influence of various factors:
- Inflammatory processes (poliomyelitis, encephalitis);
- Intoxication by neurotropic poisons (diphtheria or botulinum toxins);
- Mechanical trauma;
- Degenerative changes (e.g., in amyotrophic lateral sclerosis — ALS);
- Disorders of neuromuscular transmission (in myasthenia gravis, botulism, aminoglycoside toxicity, and other toxins).
Typically, a flaccid paralysis symptom complex develops:
- Hypotonia. Muscles become flabby and limp due to the cessation of nerve impulses and a significant decrease in axonal trophic support.
- Areflexia or Hyporeflexia. Segmental (cutaneous, tendon, periosteal) reflexes are reduced or completely absent due to denervation and disruption of the reflex arc.
- Atrophy and Hypotrophy. Occurs in the area of damage as a consequence of prolonged disuse and loss of neurotrophic influences on the muscles.
- Muscle Fiber Degeneration. Due to trophic deficiency, muscle tissue is gradually replaced by adipose and connective tissue.
- Decreased Muscle Excitability. Develops against the background of various forms of muscular dystrophy and is termed the muscle "degeneration" phenomenon.