Arterial Supply of the Thalamus: A Comprehensive Review.

The thalamus is a deep cerebral structure that is crucial for proper neurological functioning as it transmits signals from nearly all pathways in the body. Insult to the thalamus can, therefore, result in complex syndromes involving sensation, cognition, executive function, fine motor control, emotion, and arousal, to name a few. Specific territories in the thalamus that are supplied by deep cerebral arteries have been shown to correlate with clinical symptoms. The aim of this review is to enhance our understanding of the arterial anatomy of the thalamus and the complications that can arise from lesions to it by considering the functions of known thalamic nuclei supplied by each vascular territory.

Hypocretin-1 levels in the cerebrospinal fluid of patients with Percheron artery infarction with or without midbrain involvement: A case series.

BACKGROUND: Bilateral paramedian thalamic infarctions (BPTIs) due to artery of Percheron occlusion are known to cause hypersomnia. However, the role of hypocretin-1, a wake-promoting peptide that is located at the lateral hypothalamus, in hypersomnia in these patients remains unclear. METHODS: To clarify the role of hypocretin-1 in hypersomnia in patients with BPTIs, hypocretin-1 levels in the cerebrospinal fluid (CSF) were measured in 6 patients with BPTIs: 2 with rostral midbrain involvement (BPT+RMI) and 4 without midbrain involvement (BPT-MI). RESULTS: CSF hypocretin-1 levels were decreased in 2 patients with BPT+RMI and were within normal ranges in 4 patients with BPT-MI. Hypersomnia was noted in all the patients. In one BPT+RMI patient, hypersomnia was improved within 2 weeks and decreased CSF hypocretin-1 levels were reversed (acute phase (on day 9), 109.2 pg/mL; chronic phase (at 3 months), 323 pg/mL), whereas another BPT+RMI patient who displayed coma in the acute phase had decreased CSF orexin levels (107 pg/mL) at day 49 and exhibited severe disability. CONCLUSION: Hypocretin deficiency was not involved in hypersomnia observed in BPT-MI patients; however, CSF hypocretin-1 levels were reduced in BPT+RMI patients. Reduced CSF hypocretin-1 levels in the chronic phase may possibly predict a poor clinical outcome in patients with Percheron artery infarction.

[Case of defective route finding following right anterior thalamic infarction].

Defective route finding is a symptom in which an indivisual demonstrates inhibility to find the way in the familiar places. This symptom arises from lesions at the right parieto-occipital region and the right posterior part of the splenium of the corpus callosum. We present a case of defective route finding resulting from the right anterior thalamic infarction. A 63-year-old right-handed man abruptly presented with difficulty in route finding on his way home. Neither spatial neglect nor agnosia was observed with pictures of his house and surrounding streets. Although there was an attention disturbance, his activities of daily living were spared. Brain MRI revealed a fresh infarction at the right anterior nucleus of the thalamus. Single photon emission computed tomography using 123I-methyltyrosine showed hypoperfusion at the right parieto-occipital region as well as the right thalamus. Neuropsychological tests showed visuospatial memory disturbance. To our knowledge, this is the first report of defective route finding caused by the right anterior thalamic infarction. The right anterior thalamic nucleus might be involved in the visuospatial recognition circuit.

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.

Dysexecutive syndrome following anterior thalamic ischemia in the dominant hemisphere.

In the article, we describe a rare case: a 52-year-old male patient with an isolated lesion of the anterior thalamic nuclei in the dominant hemisphere due to an ischemic stroke. The patient's syndrome of disordered verbal fluency, working memory, learning and executive functions is seen as a part of a lesion in the dorsolateral complex circuit. During the following 6 months, we observed significant improvement in visual learning, recent memory and categorisation of subjects, while verbal learning and visuospatial planning remained insufficient. In this context, the preservation of thalamic structures in different types of cognitive deterioration is discussed.

A lesion of the anterior thalamus producing dystonic tremor of the hand.

BACKGROUND: Thalamic tremor is typically characterized by resting and intention components; a postural element is often present as well. Previously reported cases of acquired thalamic tremor have demonstrated lesions in the posterior thalamus or dentatorubrothalamic tract. OBJECTIVES: To report a case of dystonic-postural tremor of the upper extremity that occurred after a contralateral anterior thalamic infarct, and to discuss potential tremorigenic mechanisms. DESIGN: Case report. SETTING: Municipal hospital neurology clinic. PATIENT: A 65-year-old right-handed woman suddenly developed a dystonic tremor in her left hand after undergoing coronary bypass surgery. The tremor persisted unchanged for 8 months, at which time she was evaluated by us. Cranial magnetic resonance imaging scans demonstrated a right anterior thalamic infarct. CONCLUSION: To our knowledge, this is the first report of focal tremor caused by a lesion of the anterior thalamus.