Bilateral paramedian thalamic artery infarcts: report of eight cases.

Eight consecutive patients with CT scan evidence of a bilateral infarct in the territory of the paramedian thalamic artery are reported. In seven cases the infarct also extended to the territory of the polar artery. The main symptoms were: disorder of vigilance which cleared in a few days, and hypersomnolence which lasted longer and in two patients was still present a year later; amnesia, detectable clinically in four patients and only with tests in two patients, which persisted in one patient for three years; changes of mood and bulimia present in five and four patients respectively; and vertical gaze paresis in five patients. Only one patient died, and in the remainder the symptoms tended to subside, but none of the patients who could be followed-up for a year returned to normal behaviour. Clinical and CT scan correlations pointed to the mammillo-thalamic tract as the structure whose damage was responsible for the memory disorders.     

Bilateral paramedian thalamic infarction with hypothalamic dysfunction

Unilateral thalamic lesions cause transient or permanent behavioral, sensory and oculomotor disturbances; bilateral lesions of thalamus result in more severe and longer lasting symptoms. We present an atypical case of bilateral paramedian thalamic infarct with concomitant hypothalamic dysfunction. The only risk factor of ischaemic stroke found in the patient was a short lasting episode of atrial fibrillation. Bilateral paramedian thalamic infarcts may result from occlusion of one paramedian thalamic artery, which arises from the posterior cerebral artery, either with separated or with a common trunk, thus supplying the thalamus bilaterally. Independently of anatomical variants of thalamus blood supply, the most probable cause of infarct in our patient was unilateral or bilateral occlusion of the posterior cerebral artery by cardioembolism, probably in the course of basilar artery occlusion. Hypothalamic dysfunction may accompany thalamic infarcts; thus hypothalamo-pituitary function should be routinely assessed in bithalamic infarcts.     

Complex movement disorders following bilateral paramedian thalamic and bilateral cerebellar infarcts.

Complex movement disorders (CMD; including tremor, dystonias, choreoatheosis, and myoclonus) following infarcts in the posterior and posterolateral thalamic nuclei have been reported. This case of a 59-year-old man who developed CMD following bilateral paramedian and bilateral cerebellar infarcts illustrates the lack of anatomic specificity and the diverse pathophysiology which may underlie CMD.     

Bilateral thalamic infarcts with abnormal movements and permanent amnesia

A 45 year-old woman with mitral valve disease developed bilateral thalamic infarcts presenting as vigilance disorders, with mutism and downwards gaze paralysis during several days, followed by involuntary rhythmic movements over 13 days. These movements affected the four limbs with a rhythm variable with time as alternate or synchronized agonist-antagonist periods. Subsequent examinations demonstrated global, lasting amnesia and a subclinical disorder of vertical ocular movements. Repeat CT scan confirmed the presence of bilateral anterior thalamic infarcts affecting polar and/or paramedian territories. Emphasis is placed on the similarity of the abnormal movements in this case with L-dopa induced involuntary movements.     

Bilateral paramedian thalamic infarction with persisting signs of frontal lobe dysfunction

Cognition and behavior of a 46-year-old woman with a bilateral paramedian thalamic infarction is discussed with regard to dysfunctions of executive behaviors associated with frontal lobe function. The patient displayed marked disturbances in traditional neuropsychological tests measuring frontal lobe functions, as well as in attentional and mnemonic tasks depending on strategic behavior or on response flexibility, response shifting, or response inhibition. Behaviorally, the patient showed considerable apathy, confusion and perseverative tendencies in the acute state, and a diminished psychic self-activation in the chronic state. In spite of long-lasting rehabilitation efforts, the patients' neurobehavioral deficits remained and became obvious in situations with high cognitive demands.     

Bilateral paramedian thalamic syndrome: abnormal circadian wake-sleep and autonomic functions

OBJECTIVES: To describe wake-sleep and body core temperature (t degrees ) rhythm abnormalities in two patients with bilateral paramedian thalamic calcifications. METHODS: Patients underwent (18F)FDG PET scans and 24 hour polygraphic recordings of wake-sleep and t degrees. RESULTS: PET showed bilateral thalamic hypometabolism in both patients with additional basal ganglia or mesiolateral frontal and cingular hypometabolism. Wake-sleep studies showed abnormal sleep organisation and in the case with frontal and limbic PET hypometabolism, pre-sleep behaviour associated with "subwakefulness" EEG activities, lack of EEG spindles and K complexes, and features of status dissociatus. The t degrees rhythms showed increased mesor in both (37.4 degrees C and 37.75 degrees C) and inverted rhythm in one patient. CONCLUSIONS: Paramedian thalamic structures and interconnected, especially frontal and cingular, areas play a part in the organisation of the wake-sleep cycle and attendant autonomic functions.     

Bilateral paramedian thalamic infarction: a case with MRI and gamma-emission tomography

A 41-year-old woman presented with a history of sudden onset of a dementia with frontal signs and antero-retrograde amnesia. CT showed a bilateral paramedian thalamic infarct which was confirmed by MRI. The study of regional cerebral blood flow showed a decrease in both frontal regions. Results of imaging suggested lesions of the ventro-oral, latero-polar and intralaminar nuclei as well as of the mammillo-thalamic tract. The dorso-median nucleus appeared to be relatively spared.     

Bilateral thalamic pain secondary to bilateral thalamic infarcts relieved by a further unilateral ischaemic episode

This study reports a patient with severe, debilitating bilateral thalamic pain caused by bilateral thalamic infarcts. The authors consider it to be a unique case as a further clinically unilateral lesion led to pain relief bilaterally.     

Lateral thalamic infarcts

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.     

Rendu-Osler-Weber syndrome presented paramedian thalamic and midbrain infarcts and primary medullary hemorrhage: a case report

We reported a 41-year-old male with paramedian thalamic and midbrain infarcts due to cerebral embolism from bilateral pulmonary arterio-venous fistula and primary medullary hemorrhage. The patient had an episode of sudden onset consciousness disturbance with left Weber's syndrome (right hemiplegia and left oculomotor palsy) and vertical gaze palsy at age of 23. He noticed numbness in the left hand and the left half body under clavicular when he had got up in a morning at age 41. He had headache and left tinnitus on second and third days, and on the 3rd and 4th days, he experienced nausea. He had severe hiccup persisting from the 6th to the 13th days. The 23rd days he was admitted to our hospital. He showed dysesthesia and paresthesia in left half body under clavicular, dysesthesia in left hand and vertical gaze palsy and convergence disturbance. MRI performed on the 18th and 24th days, disclosed hyperdense mass in T1 and T2-weighted images in dorsal site of medulla, but the 70th days MRI showed no abnormal lesions. Therefore we diagnosed the high intensity mass as primary medullary hemorrhage. Cerebral angiography showed no abnormal vasculature. Many members of his family had history of sever nasal bleeding. He had skin hemangioma and mucosal hemangioma in esophagus, stomach, colon and rectum, and bilateral pulmonary arterio-venous fistula which had been operated at age 39. His mother also had skin hemangioma and pulmonary arterio-venous fistula. Therefore this family was diagnosed Rendu-Osler-Weber syndrome (hereditary hemorrhagic telangiectasia). MRI also disclosed multiple cerebral infarctions in bilateral thalamus, left cerebral peduncle and left cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)     

'Peduncular hallucinosis' following paramedian thalamic infarction

An 83-year-old man had the sudden onset of vivid formed hallucinations, agitation, and sleep disturbance suggesting "peduncular hallucinosis." A magnetic resonance scan revealed a right paramedian thalamic infarction with no abnormality of the cerebral peduncles or midbrain.     

Total recovery after bilateral paramedian thalamic infarct

Bilateral paramedian thalamic infarcts are characterised initially by the association of acute vigilance disorders and vertical gaze palsy, followed by persisting dementia with severe mnemic disturbance, global aspontaneity and apathy. We describe a patient with a dramatic neuropsychological recovery, confirmed by testing examination and completed by a cerebral metabolism study. The pathophysiology of this type of cognitive deficit is discussed.     

The syndrome of bilateral paramedian thalamic infarction

Bilateral anterior paramedian thalamic infarction resulting from occlusion of a bilaterally distributed thalamosubthalamic paramedian artery was demonstrated on CT in two patients. Patient 1 presented with a transient coma followed by asterixis, hypersomnia, vertical gaze disturbances, profound Korsakoff amnesic syndrome, and a subcortical dementia. Patient 2, with a predominantly right-sided thalamic infarct, showed good recovery from amnesia and vertical gaze disturbances. However, patient 1 remained with severe amnesia and mild subcortical dementia at follow-up 1 year later. These and similar reported cases constitute a lacunar syndrome with characteristic clinical and CT features.     

Monocular central dazzle after thalamic infarcts.

The authors observed a patient after he had ischemic strokes in both paramedian thalamic regions, which were more marked on the left side. Symptoms included dysphasia, vertical binocular diplopia, right-sided hemianopia, and a right-sided sensory and motor deficit, sparing the face. However, the most disturbing phenomenon was a painless, left monocular dazzle, which was the presenting symptom and also the only persisting symptom. This report shows that a thalamic lesion may be at the origin of central dazzle, and to the authors' knowledge, it is the first clinical observation of its monocular occurrence. It is conceivable that this dazzle was due to optic-trigeminal summation.     

Severe personality changes after unilateral left paramedian thalamic infarct

Personality changes are not uncommon after paramedian thalamic infarction, but usually bilateral or relatively large lesions, often complicated by other neurological or neuropsychological deficits, are present. 'Pure' cases of unilateral lesions are extremely rare. We report that a right-handed, 48-year-old man, who was hypertensive and diabetic but had no prior psychiatric history, developed severe personality changes and a frontal-like syndrome after recovery from acute-onset impairment of consciousness at the age of 43. Other neurological and neuropsychological disturbances, especially verbal and visual amnesia, were unremarkable. MRI showed a very small infarct in the left paramedian area of the thalamus, mainly involving the dorsomedial nucleus.     

The syndrome of combined polar and paramedian thalamic infarction

BACKGROUND: Occlusion of the polar or the paramedian arteries of the thalamus usually leads to distinct infarcts with specific clinical and imaging correlates. However, vascular variation is such that in up to one third of humans, the polar artery is missing and its territory taken over by the paramedian arteries. OBJECTIVE: To provide attention to the corresponding stroke syndrome of combined polar and paramedian thalamic infarction. METHODS: We studied combined polar-paramedian thalamic infarction in 12 patients (6 right-sided lesions, 3 left-sided lesions, and 3 bilateral lesions) who were selected from 208 consecutively registered patients with thalamic strokes in the Lausanne Stroke Registry. RESULTS: The clinical manifestation included executive dysfunction, apathy, and memory impairment in all patients, with eye movement disturbances in 10 patients (5 with right-sided lesions, 2 with left-sided lesions, 3 with bilateral lesions); acutely impaired consciousness in 11 patients (5 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions); aphasic disturbances in 8 patients (2 with right-sided lesions, 3 with left-sided lesions, 3 with bilateral lesions), including nonfluent aphasia in 1 patient (with left-sided lesions); dysarthria in 5 patients (4 with right-sided lesions, 1 with bilateral lesions); constructional apraxia in 5 patients (with right-sided lesions); mild hemiparesis in 4 patients (2 with right-sided lesions, 2 with left-sided lesions); dyscalculia in 3 patients (1 with left-sided lesions,1 with right-sided lesions, 1 with bilateral lesions); limb dystonia or asterixis in 2 patients (1 with right-sided lesions, 1 with bilateral lesions); mild hemisensory loss in 2 patients (1 with right-sided lesions, 1 with left-sided lesions); hemiataxia in 1 patient (with right-sided lesions); and ideomotor apraxia in 1 patient (with left-sided lesions). Follow-up showed severely disabling, persistent amnesia in 7 patients (4 with right-sided lesions, 3 with bilateral lesions) and persistent eye movement dysfunction in 5 patients (2 with right-sided lesions, 1 with left-sided lesions, 2 with bilateral lesions). The most common etiology appeared to be cardioembolism, followed by artery-to-artery embolism and presumed small-artery disease. CONCLUSIONS: Key features of this syndrome included amnesia preceded by a period of altered consciousness, and vertical eye movement disturbances. The severe and persistent amnesia may be due to coexisting damage to the anterior and dorsomedial nuclei.     

Life-threatening bradycardia after bilateral paramedian thalamic and midbrain infarction

Journal of Neurology -