[Gustatory nervous pathway syndromes]. / Síndromes lesionales de las vías nerviosas gustativas.

Although the lingual nerve and the chorda tympani are the components of the classic peripheral gustatory pathway, loss of taste in patients after surgery for trigeminal neuralgia supports for the existence of an accessory gustatory pathway through the trigeminal sensory root and the gasserian ganglion. Bell's palsy is the most common pathology of the peripheral gustatory pathway. The central gustatory pathway ascends from the solitary tract nucleus in the medulla up to the upper pons in the ipsilateral central tegmental tract, rather than in the medial lemniscus as proposed in the past. It is not possible to specify whether the central gustatory pathway decussates or not at the lower midbrain level. Interruption of the gustatory pathway in the brainstem usually occurs with stroke or demyelination. The thalamic gustatory relay is located in the most medial aspect of the ventroposteromedial nucleus, immediately adjacent to the somatosensory area for the oral cavity and fingers. Therefore, ageusia associated with the sensory cheiro-oral syndrome may occur with a thalamic lesion. The laterality of the gustatory representation in the thalamus remains unresolved. Studies on epileptic gustatory aura have demonstrated that the insula and the anteromedial temporal lobe are the primary and secondary gustatory cortex, respectively. Taste perception results in patients with corpus callosum section and strokes or tumors involving the insula support the hypothesis that there is a gustatory representation of both hemitongues in the left cerebral hemisphere, whereas only the right hemitongue is represented in the right hemisphere.

Síndromes lesionales de las vías nerviosas gustativas / Gustatory nervous pathway syndromes

La vía nerviosa gustativa periférica está fundamentalmente constituida por el nervio lingual y la cuerda del tímpano, pero diferentes observaciones clínicas (ageusia poscirugía de la neuralgia trigeminal) abogan por la existencia de una vía periférica accesoria a través de la raíz trigeminal y del ganglio de Gasser. La parálisis de Bell es la causa más común de lesión de la vía gustativa periférica. La vía gustativa central se inicia en el bulbo con el núcleo solitario y asciende ipsilateralmente en el puente a lo largo del tracto tegmentario central y no a través del lemnisco medial, como se creía en el pasado. La decusación o no de la vía gustativa en el mesencéfalo es motivo de controversia. Las lesiones de la vía gustativa troncoencefálica suelen ser de naturaleza vascular o desmielinizante. La vía gustativa llega a la parte más interna del núcleo ventral posteromedial del tálamo, y allí está en estrecho contacto con el área que recoge la sensibilidad de la cavidad oral y de la mano. Por ese motivo, la afección de ese núcleo suele manifestarse por un síndrome sensitivo queirooral asociado a hemiageusia. La cuestión de la ipsilateralidad o contralateralidad de las proyecciones talámicas con respecto a la hemilengua estimulada no está todavía aclarada. La ínsula es el centro cortical primario del gusto y el lóbulo temporal anteromedial actuaría como un centro gustativo secundario o accesorio, según se ha demostrado en el estudio del aura gustativa epiléptica. Los resultados obtenidos en pacientes callosectomizados o con lesiones vasculares o tumorales insulares apoyan la tesis de una representación gustativa de ambas hemilenguas en el hemisferio cerebral izquierdo, mientras que la información gustativa de la hemilengua derecha sólo estaría representada en el hemisferio derecho. (AU)

Ageusia associated with thalamic plaque in multiple sclerosis.

Ageusia and the cheirooral syndrome developed in a patient with a relapse of multiple sclerosis. Magnetic resonance imaging revealed an area of demyelination in the thalamus. This lesion presumably affected the most medial part of the ventralis posterior nucleus, where taste information is located. Given the proximity of the taste area and somatosensory representation of the hand and oral cavity in the ventralis posterior nucleus, we propose that a diagnosis of thalamic lesion should be considered when ageusia occurs with the cheirooral syndrome.

Evidence of somatotopic organization of the sensory thalamus based on infarction in the nucleus ventralis posterior.

BACKGROUND: This is to describe a restricted sensory syndrome of unique distribution due to thalamic infarct. CASE DESCRIPTION: We report a case of pure sensory disturbance involving the left intraoral and perioral regions and the tips of the thumb and forefinger of the left hand. Magnetic resonance imaging revealed a small infarct in the contralateral thalamus, presumably affecting the nucleus ventralis posterior. CONCLUSIONS: This patient provides an excellent correlation between clinical findings and thalamic representation of body surface as established during stereotactic procedures.

Oral dyskinesias associated with bilateral thalamo-capsular infarction.

Involuntary mouthing movements indistinguishable from neuroleptic-induced tardive dyskinesia followed stroke in a woman whose computed tomographic (CT) scan showed bilateral thalamo-capsular infarction.

Spanish toxic oil syndrome neuropathy in three patients with hereditary motor and sensory neuropathy type I.

We describe three patients with hereditary motor and sensory neuropathy type I coming from a family who suffered from Spanish toxic oil syndrome with neuromuscular manifestations. Their clinical course neither differed from other kin only affected with the inherited neuropathy nor from other patients with Spanish toxic oil syndrome studied by us. These findings suggest that patients with hereditary motor and sensory neuropathy do not exhibit a special susceptibility to vasculitic neuropathy associated with Spanish toxic oil syndrome.