[Cerebellar infarct with complications].

BACKGROUND

Symptoms of circulatory disorders depend on the volume and localization of the cerebellar infarction. An isolated blood vessel occlusion may have various symptoms due to numerous anastomoses in the cerebellar hemispheres. Dominant symptoms are vertigo, vomiting, nausea and balance disorders. Due to a great number of anastomoses between the three cerebral arteries, if only one of them is occluded, expected symptoms rarely occur, so that vertebral angiography performed in the first 24 hours from the onset of clinical picture, points to a lesion of the cerebellar parenchyma on the basis of radiologic signs of occlusion. Further on, brain computerized tomography solves the diagnostic dilemma, but unfortunately, ischemic cerebellar lesions are often detected only in pathoanatomic findings. Development and course of cerebellar malformation are of great importance for occurrence of symptoms. Cerebellar symptoms often occur in cases of brain-stem lesions. In dorsal hemisection lesions the following symptoms occur: vertigo, vomiting, nystagmus, taste disorders and secretory trophic disorders in the gastrointestinal tract. In cases of spreading to the pyramidal neurons the following symptoms occur: a soft palate and vocal cord paresis, swallowing difficulties and disorders of phonological as well as hemiplegia and sensibility disorders.

METHODS

This is a case of a male patient, 60 years of age. He was admitted to the Neuropsychiatric Department because of high blood pressure, severe headache in the back of the head, vertigo and nausea, without vomiting. He complained about weakness in the left side of the body. The somatic status was normal. In regard to neurologic status he had a slow photomotoric reaction of pupils to light, swallowing difficulties, hoarse voice, decreased pharyngeal reflex, symmetrically fast reflexes, walk on wide basis, in Romberg position unstable, whereas other findings were normal. Psychically average. The reaction to therapy was good. Subjectively the patient felt-well, but swallowing difficulties persisted. On the seventh day from admission his status suddenly aggravated, with severe vertigo, vomiting on several occasions, weakness and high temperature, hypotension, tachycardia, left eyelid ptosis with horizontal nystagmus when looking to the left. Lung radiography revealed bilateral pneumonia; computerized tomography of the brain revealed a great ischemic zone in the left cerebellar hemisphere discretely dislocating the brain mass to contralateral side. Resistant hypotension persisted. Surgical findings of the rectum revealed a dark content. Gastroscopy revealed esophageal candidiasis; mucus bleeding was spontaneous and at touch, whereas in the lower third of esophagus there was a mucous lesion. Haematinised blood was found in the stomach and duodenum. The patient's state continually aggravated and after massive stool blood loss a surgery was performed. A great penetrating ulcer was detected at the back duodenal wall 30 mm of size, visualizing the pancreas. A final surgical procedure was performed at the Clinic for Abdominal Surgery in Novi Sad. The postoperative course was good, but on the 7th postoperative day unexpected fatal outcome occurred due to massive lung embolism. Pathoanatomic examination revealed a postencephalomalacic pseudocyst in the left cerebellar hemisphere.

CONCLUSIONS

This is a case report of a patient with lateral medullar syndrome associated with complications which can only partly be explained by the basic disease. Pneumonia and a secretory trophic disorder of the gastrointestinal tract are frequent complications that can be life threatening is spite of intensive management.