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Myopathy

Problems such as muscle weakness, fatigue, stiffness, cramps, tension, atrophy, pain, and involuntary movement do not necessarily signify disease of the muscle itself. Myopathy must be distinguished from neurogenic weakness of UMN or LMN type. Weakness may accompany systemic disease because of a generalized cata-bolic state or through a specific disease-related impairment of muscle function. Myopathy may be either primary or secondary, i.e., the product of another underlying disease. Different types of myopathy affect different muscle groups: some are generalized (congenital myopathy), while others are mainly either proximal (Duchenne type muscular dystrophy, polymyositis) or distal (myotonic dystrophy, inclusion body myositis), or mainly affect the head and face (mito-chondrial myopathy). Myasthenia gravis, strictly speaking a disorder of neuromuscular transmission rather than a form of myopathy, most prominently affects the orbicularis oculi muscle; weakness increases with exercise. Muscle power is commonly graded according to the scale proposed by the British Medical Research Council (MRC) (1976):

0 No muscle contraction

1 Visible or palpable contraction, but no movement

2 Movement occurs, but not against gravity

3 Movement against gravity

4 Movement against gravity and additional resistance

5 Normal muscle power ism), and chronic toxic myopathies (alcohol, corticosteroids, chloroquine).

■ Disorders of Muscle Function

In these disorders, weakness is due to impaired function of the muscle fibers. Persistent weakness can lead to muscle atrophy. The episodic occurrence or worsening of muscle weakness is typical.

Primary myopathies. Hypokalemia- and hyper-kalemia-related forms of paralysis belong to this group.

Myasthenic syndromes. Myasthenia gravis and Lambert-Eaton syndrome are characterized by abnormal fatigability of the muscles. Postviral fatigue syndrome. Mildly increased fatigability of the muscles may persist for weeks after recovery from a viral illness.

■ Muscle Pain and Stiffness

Muscle pain and stiffness restrict movement, causing weakness as a secondary consequence. Muscle pain. Muscle pain (myalgia, p. 346) at rest and on exertion accompanies muscle trauma (muscle rupture, strain, soreness, compartment syndromes), viral myositis (influenza, Coxsackie virus, herpes simplex virus), fibromy-algia, polymyalgia rheumatica, and muscle cramps and spasms of various causes (malignant hyperthermia, carnitine palmitoyl-transferase deficiency, phosphorylase defi-ciency/glycogen storage disease type V). Muscle stiffness. Stiffness is prominent in congenital myotonia, neuromyotonia, and cold-induced paramyotonia.

■ Muscle Atrophy

Myopathy produces atrophy through the impaired development, the destruction, and the impaired regeneration of muscle fibers. Primary (genetic) myopathies include the progressive muscular dystrophies, myotonic muscular dystrophies, congenital myopathies (e.g., central core disease, nemaline myopathy), and metabolic myopathies (Pompe disease/gly-cogen storage disease type II, Kearns-Sayre syndrome, carnitine deficiency).

52 Secondary myopathies include myositis, my-opathy due to endocrine disorders (hyperthy-roidism and hypothyroidism, hyperparathyroid-

Artery

Striated

Three primary-

bundles of muscle fibei

Progressive Duchenne muscular dystrophy

(proximal leg weakness, patients use arms to raise themselves to standing position = Gowers's sign, calf hypertrophy, lumbar hyperlordosis)

Artery

Striated

Three primary-

bundles of muscle fibei

Muscular Dystrophy Gowers Sign
Structure of skeletal muscle

Myotonic response

(delayed fist opening)

Myasthenic response

(exercise-induced muscle weakness; here in eyes)

Hyperparathyroid Pathway

Muscle pain and stiffness

(exercise-induced; here due to ischemia)

External ophthalmoplegia

(here mitochondrial myopathy)

The functions of the cerebellum include the control of balance, posture, gait, and goal-directed movement, and the regulation of muscle tone.

Neural Pathways

Afferent connections. The three large white-matter tracts (peduncles) of the cerebellum convey afferent input to the cerebellar cortex from the cerebral cortex (especially visual areas), pontine nuclei, the brain stem nuclei of the trigemi-nal, vestibular, and cochlear nerves, and the spinal cord. The superior cerebellar peduncle conveys ipsilateral proprioceptive input (p. 104) from the anterior spinocerebellar tract of the spinal cord. The middle cerebellar peduncle car-.O ries fibers of pontine origin (p. 45). The inferior u cerebellar peduncle carries fibers from the vesti-§ bular nerve and nucleus to the flocculonodular ^ lobe and fastigial nucleus, and from the con-,2 tralateral inferior olive to the cerebellar hemi-5 spheres (olivocerebellar tract), as well as propri-oceptive input from the posterior spinocerebel-lar tract (derived from muscle spindles and destined for the anterior and posterior portions of the paramedian cerebellar cortex) and fibers from the brain stem reticular formation. Efferent connections. The cerebellar nuclei (fastigial, globose, emboliform, and dentate; p. 43) project via the (contralateral) superior cerebellar peduncle to the red nucleus, thalamus, and reticular formation. The thalamus projects in turn to the premotor and primary motor cortex, whose output travels down to the pons, which projects back to the cerebellum, forming a neuroanatomical circuit. Cerebellar output influences (ipsilateral) spinal motor neurons by way of the red nucleus and rubrospinal tract. The inferior cerebellar peduncle projects to the vestibular nuclei and brain stem reticular formation (completing the vestibulocerebellar feedback loop) and influences spinal motor neurons by way of the vestibulospinal and reti-culospinal tracts.

Functional Systems

The cerebellum can be thought of as containing 54 three separate functional components.

Vestibulocerebellum (archeocerebellum). Structures: Flocculonodular lobe and lingula. Afferent connections: From the semicircular canals and maculae (p. 56), vestibular nucleus, visual system (lateral geniculate body), superior col-liculus, and striate area to the vermis. Efferent connections: From the fastigial nucleus to the vestibular nucleus and reticular formation. Functions: Control of balance, axial and proximal muscle groups, respiratory movements, and head and eye movements (stabilization of gaze). Effects oflesions: Loss of balance (truncal ataxia, postural ataxia > gait ataxia), nystagmus on lateral gaze, and absence of visual fixation suppression (p. 26) resulting in oscillopsia (stationary objects seem to move). Spinocerebellum (paleocerebellum). Structures: Parts of the superior vermis (culmen, central lobule) and inferior vermis (uvula, pyramis), parts of the cerebellar hemispheres (wing of central lobule, quadrangular lobule, parafloc-culus). Afferent connections: The pars intermedia receives the spinocerebellar tracts, projections from the primary motor and somatosensory cortex, and projections conveying auditory, visual, and vestibular information. Efferent connections: From the nucleus interpositus to the reticular formation, red nucleus, and ven-trolateral nucleus of the thalamus, which projects in turn to area 4 of the cortex. Functions: Coordination of distal muscles, muscle tone (postural control), balance, and velocity and amplitude of saccades. Effects of lesions: Gait ataxia > postural ataxia, muscular hypotonia, dysmetria.

Pontocerebellum (neocerebellum). Structures: Most of the cerebellar hemispheres, including the declive, folium, and tuber of the vermis. Afferent connections: From sensory and motor cortical areas, premotor cortex, and parietal lobes via pontine nuclei and the inferior olive. Efferent connections: From the dentate nucleus to the red nucleus and the ventrolateral nucleus of the thalamus, and from these structures onward to motor and premotor cortex. Functions: Coordination, speed, and precision of body movement and speech. Effects oflesions: Delayed initiation and termination of movement, mistiming of agonist and antagonist contraction in movement sequences, intention tremor, limb ataxia.

Fastigial nucleus Reticular formation

Uvula

Uvula

Spinocerebellum

Postural and gait ataxia

Thalamocortical tract Central lobule Thalamus

(ventral lateral nucleus)

Red nucleus Reticular formation Rubrospinal tract

Spínocerebeiium

Emboliform and globose nuclei

— Reticulospinal tract

— Spinocerebellar tract

Fastigial nucleus Reticular formation

Spínocerebeiium

Areas S and l

-Area 4

Postural and gait ataxia

Thalamocortical tract Central lobule Thalamus

(ventral lateral nucleus)

Emboliform and globose nuclei

Red nucleus Reticular formation Rubrospinal tract

— Reticulospinal tract

— Spinocerebellar tract

Spinocerebellum

Areas S and l

-Area 4

Spinocerebellum

Rubrospinal Tract Red Nucleus

Hemisphere

Pontocere-bellum

Hemisphere

Olive

Rubrospinal tract

Pontocerebeiium

Structure of cerebellum

(overview; median section of vermis right)

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  • rhea
    What are proximal leg muscles?
    8 years ago

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