Classification of motor disorders
Depending on which specific structures of the nervous system are damaged, there are four main types of paralysis and paresis:
- Central (also known as pyramidal or spastic);
- Peripheral;
- 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. At the same time, the amplitude of the reflex response increases significantly, and reflexogenic zones expand.
- Muscle hypertonia of the spastic type. Tone in central paralysis increases unevenly. A typical distribution is formed: in the arm, spasticity predominates in the adductor muscles of the shoulder and flexors of the forearm; in the leg, the extensors of the thigh and leg, the adductors of the thigh, and the flexors of the foot are tense. Over time, such persistent movement restriction leads to the fixation of the limb in an unusual position — neurogenic contractures develop.
- Pathological reflexes. Subdivided into flexor and extensor ones (e.g., Babinski, Rossolimo, Bechterew reflexes). Extensor reflexes serve as one of the earliest and most constant signs of pyramidal tract damage.
- Clonus. Represents an extreme, high degree of severity of tendon-muscle reflexes. Clinically, it looks like a series of rapid rhythmic muscle contractions (spontaneous or in response to stimulation). Most commonly observed as foot, patellar, hand, or jaw clonus.
- Syncinesias. These are involuntary associated muscle contractions. They occur in the paralyzed limb when the patient performs a conscious movement with the healthy limb or another part of the body. They are mediated by the participation of the spinal cord, cerebellum, and pyramidal system.
Extrapyramidal disorders (rigidity)
When the extrapyramidal system is damaged (which is typical, for example, for parkinsonism), a different type of tone change develops — rigid paresis. Its pathogenetic mechanism consists of a simultaneous increase in tone in both flexors and extensors.
Clinically, this is manifested by the "lead-pipe rigidity" phenomenon: the patient's torso or limb is able to maintain the posture imparted to it from the outside for a long time.
Peripheral (flaccid) paralysis
The pathogenetic basis of peripheral paralysis is primary (hereditary, congenital) or acquired lesions of the peripheral motor neurons themselves (cells of the anterior horns of the spinal cord, cranial nerve nuclei).
Acquired injuries develop under the influence of various factors:
- Inflammatory processes (poliomyelitis, encephalitis);
- Intoxication by neurotropic poisons (diphtheria or botulinum toxins);
- Mechanical trauma;
- Degenerative changes (for example, in amyotrophic lateral sclerosis — ALS);
- Neuromuscular transmission disorders (in myasthenia gravis, botulism, the action of aminoglycoside antibiotics and other toxins).
In typical cases, a flaccid paralysis symptom complex forms:
- Hypotonia. Muscles become flabby and flaccid due to the cessation of nerve impulses and a significant decrease in axonal nutrient supply.
- Areflexia or hyporeflexia. Segmental (cutaneous, tendon, periosteal) reflexes are reduced or completely lost due to denervation and rupture 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.
- Degeneration of muscle fibers. 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 designated by the term muscle "degeneration" phenomenon.
Briefly: answers to topical questions
Which pathological reflexes are classified as extensor reflexes in central paralysis?
Extensor pathological reflexes in central paralysis include the Babinski reflex, as well as Oppenheim and Gordon signs.
- Babinski reflex (Babinski reflex) — slow tonic extension of the big toe with simultaneous fan-like divergence of the other toes in response to stroking the skin of the outer edge of the sole.
- Oppenheim sign — extension of the big toe when running a finger down the anterior surface of the tibia from top to bottom.
- Gordon sign — reflexive extension of the big toe, occurring in response to circular compression of the calf muscle.
Which pathological reflexes are classified as flexor reflexes in central paralysis?
Flexor pathological reflexes in pyramidal tract damage include the Rossolimo reflex in the lower extremity and the Trömner reflex in the upper extremity.
- Rossolimo reflex (Rossolimo reflex) — rapid plantar flexion of the toes, occurring in response to short, sharp strikes on the plantar surface of the distal phalanges of toes II–V.
- Trömner reflex (Trömner reflex) — a pathological hand reflex (the hand equivalent of the Rossolimo reflex), manifested by flexion of the terminal phalanges of the hand fingers upon a quick strike from bottom to top on the palmar surface of the terminal phalanx of the III finger.
Class and exam questions
What is the difference between muscular hypertonia in central and extrapyramidal paresis?
In central paralysis, tone increases unevenly (predominantly in the flexors of the arm and extensors of the leg). In extrapyramidal damage, tone increases simultaneously in both flexors and extensors, causing the "lead-pipe rigidity" effect.
Why do pathological reflexes and hyperreflexia occur in central paralysis?
They are caused by the disinhibition (increased activity) of segmental reflexes of the spinal cord. This happens due to the weakening or complete loss of inhibitory descending influences from the brain.
What is the earliest sign of pyramidal tract lesion?
One of the earliest and most constant signs of pyramidal system damage is the appearance of extensor pathological reflexes (e.g., the Babinski reflex).
What does untreated spastic hypertonia lead to over time?
Prolonged spastic hypertonia is complicated by the development of neurogenic contractures — persistent limitation of movement in the joints, causing the limb to be rigidly fixed in a pathological position.
What else to study on this topic
- Pathological reflexes (Babinski, Rossolimo, Bechterew): elicitation technique and evaluation
- Mechanism of formation and prevention of neurogenic contractures
- Amyotrophic lateral sclerosis (ALS) as a cause of motor neuron degeneration
- Effect of aminoglycoside antibiotics on neuromuscular transmission
- The phenomenon of muscle "degeneration" in flaccid paralysis
Master the entire topic in the "Pathophysiology" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Central paralysis and paresis" and 4,913 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 135 video lessons on the subject
Other topics in "Chapter 28. Standard forms of pathology of the nervous system"
Free video lessons: pathophysiologyShort lessons with lecture notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.