Symptoms of medulla oblongata lesions

The medulla oblongata is a continuation of the spinal cord and has similar structural features - it consists of conducting pathways and nuclei. In front, it borders the pons, and behind, without a clear border, it passes into the spinal cord (the lower edge of the medulla oblongata is conventionally considered to be the decussation of the pyramids or the upper border of the first cervical spinal roots).

On the ventral surface of the medulla oblongata is the anterior median fissure, with pyramids on either side. Outside the pyramids are the inferior olives, separated from them by the lateral anterior groove. On the dorsal surface of the medulla oblongata below the rhomboid fossa are the posterior funiculi (thin and cuneate bundles), separated by an unpaired posterior medial groove and paired posterolateral grooves. The dorsal surface of the anterior section of the medulla oblongata forms the floor of the ventricle (the posterior angle of the rhomboid fossa). Outside its edges on the lateral surface of the medulla oblongata are the inferior cerebellar peduncles.

In the transverse section of the medulla oblongata, the pyramidal tract passes in its ventral section, and the fibers of the decussation of the medial loop are located in the central part (they conduct impulses of deep sensitivity from the nuclei of the thin and cuneate fasciculi to the thalamus). The ventro-lateral sections of the medulla oblongata occupy the inferior olives. Dorsal to them are the ascending conductors that form the inferior cerebellar peduncles, as well as the spinothalamic fasciculus. In the dorsal section of the medulla oblongata, there are nuclei of the posterior group of cranial nerves (XX pair), as well as a layer of the reticular formation.

The nuclei of many cranial nerves are located in the floor of the 5th ventricle (rhomboid fossa). At the level of the lower (posterior) angle are the nuclei of the hypoglossal (medially) and vagus nerves (laterally). At the level of the outer angle of the rhomboid fossa, parallel to the median groove, lies the sensory nucleus of the trigeminal nerve, lateral to it are the vestibular and auditory nuclei, and medial is the nucleus of the solitary tract (the taste nucleus of the glossopharyngeal and vagus nerves). Paramedian to the front of the hypoglossal nerve nucleus are the motor nucleus of the glossopharyngeal and vagus nerves and the salivary nuclei.

Syndromes of damage to the medulla oblongata: symptoms of dysfunction of the nuclei and roots of the X, X, X and X pairs of cranial nerves, the inferior olive, the spinothalamic tract, the nuclei of the thin and cuneate fasciculi, the pyramidal and descending extrapyramidal systems, the descending sympathetic fibers to the ciliospinal center, the posterior and anterior spinocerebellar tracts.

The main alternating syndromes are the following.

Avellis syndrome: peripheral paralysis of half of the tongue, soft palate and vocal cord (X, X, X pairs of cranial nerves) on the side of the lesion and hemiplegia on the opposite side; develops with a lesion in one half of the medulla oblongata.

Jackson syndrome: peripheral paralysis of the tongue muscles on the affected side and central paralysis of the opposite limbs occurs when one pyramid of the medulla oblongata and the root of the X pair of cranial nerves are affected.

Wallenberg-Zakharchenko syndrome: damage to the vagus nerve on the side of the lesion (unilateral paralysis of the soft palate, vocal cord, swallowing disorder; on the same side, Bernard-Horner symptom, cerebellar ataxia, facial anesthesia, dissociated anesthesia on the opposite side (alternating hemianesthesia); occurs with impaired blood circulation in the vertebral artery or the inferior posterior cerebellar artery extending from it; the ischemic lesion is located in the dorsolateral part of the medulla oblongata.

Schmidt syndrome: on the side of the lesion there is paresis of the vocal cord, soft palate, trapezius and sternocleidomastoid muscles; on the opposite side there is spastic hemiparesis, i.e. the nuclei and fibers of the IX, X, XI, XII pairs of cranial nerves and the pyramidal system are affected.

Tapia syndrome: on the affected side there is paralysis of the trapezius, sternocleidomastoid muscles (accessory nerve) and half of the tongue (hypoglossal nerve), contralateral spastic hemiparesis.

Voplestein syndrome; on the side of the lesion there is paresis of the vocal cord due to damage to the nucl. ambiguus, contralaterally - hemianesthesia of superficial sensitivity (spinal-thalamic tract).

Babinski-Nageotte syndrome: on the affected side - cerebellar symptoms (ataxia, nystagmus, asynergy), Claude Bernard-Horner syndrome, hyperthermia; contralateral spastic hemiparesis, dissociated hemianesthesia (loss of pain and temperature sensitivity); the syndrome is caused by damage to the posterolateral part of the medulla oblongata and the pons.

Glick's syndrome: characterized by combined damage to the V, V, X nerves and the pyramidal system; on the affected side - loss of vision (or amaurosis), pain in the supraorbital region, paresis of the facial muscles, difficulty swallowing; contralaterally - spastic hemiparesis.

With bilateral damage to the nuclei and roots of the X, X and X pairs of cranial nerves, bulbar paralysis develops. It is characterized by impaired swallowing (choking, liquid food getting into the nose), changes in the sonority of the voice (hoarseness, aphonia), the appearance of a nasal tone of speech (nasolalia), dysarthria. Atrophy and fascicular twitching of the muscles of the tongue are observed. The pharyngeal reflex disappears. This syndrome most often occurs in vascular and some degenerative diseases (amyotrophic lateral sclerosis, syringobulbia).

Pseudobulbar palsy is a central paralysis of the muscles innervated by the X, X, X pairs of cranial nerves. It develops with bilateral damage to the cortico-nuclear tracts. The foci are located at different levels above the medulla oblongata, including the brainstem. Clinical manifestations are similar to those of bulbar palsy (difficulty swallowing, nasal voice, dysarthria). With pseudobulbar palsy, reflexes of oral automatism (proboscis, palmar-chin, tongue-labial, etc.), forced laughter and crying appear. Signs of damage to the peripheral neuron (atrophy, fascicular twitching, etc.) are absent. The syndrome is most often associated with vascular lesions of the brain.

Thus, pathological foci in the brainstem may involve the pyramidal system and motor nuclei of the cranial nerves. In addition, this may damage the sensory conductors, as well as the nuclei and roots of the sensory cranial nerves. At the same time, the brainstem contains nerve formations that have activating and inhibitory effects on large areas of the brain and spinal cord. This refers to the function of the reticular formation of the brainstem. It has wide connections with the lower and higher parts of the brain. Numerous collaterals from specific sensory pathways approach the reticular formation. Impulses pass through it that tone the cortex and subcortical formations and ensure their activity and the waking state of the brain. Inhibition of ascending activating influences leads to a decrease in the tone of the cortex and the onset of drowsiness or true sleep. Along the descending pathways, the reticular formation sends impulses that regulate muscle tone (increases or decreases).

The reticular formation includes separate areas with a certain specialization of functions (respiratory, vasomotor and other centers). The reticular formation is involved in maintaining a number of vital reflex acts (breathing, cardiovascular activity, metabolism, etc.). In case of damage to the brainstem, especially the medulla oblongata, in addition to those described above, one must also encounter such severe symptoms as respiratory and cardiovascular disorders.

When the function of the reticular formation is disrupted, sleep and wakefulness disorders develop.

Narcolepsy syndrome: attacks of the patient's uncontrollable desire to fall asleep in a completely inappropriate environment (during a conversation, eating, walking, etc.); paroxysms of narcolepsy are often combined with paroxysmal loss of muscle tone (cataplexy), which occurs during emotions, which leads to the patient's immobility for several seconds or minutes; sometimes there is an inability to actively move for a short period of time immediately after awakening from sleep (cataplexy of awakening, or "night paralysis").

There is another type of sleep disorder - the syndrome of "periodic hibernation": attacks of sleep lasting from 10-20 hours to several days, Kleine-Levin syndrome: attacks are accompanied by bulimia. Thus, the reticular formation can participate in the formation of syndromes that occur when the focus is localized not only in the trunk, but also in other parts of the brain. This emphasizes the existence of close functional connections according to the principle of neuronal circles, including cortical, subcortical and trunk structures.

In case of pathological foci outside the brainstem (extratruncally), several closely located nerves may suffer, and characteristic syndromes arise. Among them, it is important to note the pontocerebellar angle syndrome - damage to the auditory, facial and trigeminal nerves. It is characteristic of neurinoma of the V pair of cranial nerves and basal arachnoiditis.

Internal auditory canal syndrome (Lyanits' syndrome): damage to the auditory nerve, tinnitus, hearing loss in the sound-perceiving type), facial nerve (peripheral paralysis of the facial muscles, dry eyes, decreased taste in the anterior third of the tongue) on the side of the lesion; also occurs with neuroma of the 5th pair of cranial nerves.

Gradenigo-Lannoy syndrome (temporal bone apex syndrome): pain in the trigeminal nerve innervation zone (irritation of the trigeminal ganglion), paralysis of the external rectus muscle of the eye on the side of the lesion; appears with inflammation of the middle ear and with a tumor localized in the middle cranial fossa.

In the case of tumor-related extratruncal lesions, conduction disorders also occur in subsequent stages of the disease due to compression of the brain stem.

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