Mesial Thalamus Research Articles

SUN-596 A Rare Presentation of Early Onset Wernicke Encephalopathy Following Sleeve Gastrectomy

Background: Wernicke encephalopathy (WE) has been reported after malabsorptive bariatric surgeries but is an uncommon complication of sleeve gastrectomy. Since 2011, the number of patients receiving a sleeve gastrectomy has tripled, with almost 60% of patients undergoing bariatric surgery receiving a sleeve gastrectomy in 2017 (1). We present a case of WE in a young woman as a rare and early complication of sleeve gastrectomy. Clinical Case: A 32-year old female with a past medical history significant for hypertension, pseudotumor cerebri, and morbid obesity status post sleeve gastrectomy two months prior presented to the emergency department with complaints of blurry vision and lower extremity numbness. Physical examination showed sluggish light reflex and decreased extraocular movements. Given history of pseudotumor cerebri, patient underwent a therapeutic lumbar puncture with removal of 13 ml of CSF. Opening pressure was 20 cm of water and patient experienced no relief of her symptoms. Ophthalmology consult did not offer an explanation for the blurry vision. MRI-brain with and without contrast showed findings highly suggestive of WE. It showed faint linear symmetric hyperintensities along the bilateral mesial thalamus, dorsal midbrain and periaqueductal gray matter, which were determined to be acute in nature in comparison with a MRI performed three weeks prior. Upon further investigation, thiamine level was low at 43.6 nmol/L [66.5 – 200] confirming the diagnosis of WE. Thiamine supplementation was started immediately and patient reported improvement of her vision the next day with return to baseline in 3 days. Conclusion: There have been a handful of cases of WE reported in literature as a complication of sleeve gastrectomy. Zheng, L also reported a case of WE 7 weeks after sleeve gastrectomy (2). Although sleeve gastrectomy does not directly affect the primary absorptive pathway of thiamine in the gastrointestinal tract, it is imperative to consider WE in patients presenting with suspicious neurologic symptoms after a recent sleeve gastrectomy. WE was suspected in our case due to typical MRI findings and neurological presentation after bariatric surgery, which was later confirmed by low serum thiamine level. Early detection and thiamine supplementation resulted in complete reversal of symptoms in our patient. WE is a rare but severe and preventable consequence of bariatric surgery that warrants attention given its rapid onset and detrimental course. Reference: (1) Estimate of Bariatric Surgery Numbers, 2011-2017. (2018, June 26). Retrieved from https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers. (2) Zheng, L. (2016).Wernicke Encephalopathy and Sleeve Gastrectomy. American Journal of Therapeutics, 23(6).

Decreased Cerebral Blood Flow in Mesial Thalamus and Precuneus/PCC during Midazolam Induced Sedation Assessed with ASL.

While some previous work suggests that midazolam-induced light sedation results from the functional disconnection within resting state network, little is known about the underlying alterations of cerebral blood flow (CBF) associated with its effects. A randomized, double-blind, within-subject, cross-over design was adopted, while 12 healthy young volunteers were scanned with arterial spin-labeling (ASL) perfusion MRI both before and after an injection of either saline or midazolam. The contrast of MRI signal before and after midazolam administration revealed the CBF decrease in the bilateral mesial thalamus and precuneus/posterior cingulate cortex (PCC). These effects were confirmed after controlling for any effect of injection as well as head motions. These findings provide new evidences that midazolam-induced light sedation is related to the disruption of cortical functional integration, and have new implications to the neural basis of consciousness.

Beta-CIT SPECT demonstrates blockade of 5HT-uptake sites by citalopram in the human brain in vivo.

The cocaine analogue 2-beta-carbomethoxy-3-beta-(4-iodophenyl)-tropane (beta-CIT) is a potent ligand for both dopamine- and serotonin uptake sites which in its 123I labeled form can be used for single photon emission computerized tomography (SPECT). It was demonstrated previously by SPECT-studies in non-human primates that 123I-beta-CIT binds to dopamine transporters in the striatum and to serotonin transporters in hypothalamus and midbrain. The aim of the present study was to compare 123I-beta-CIT binding in the brain stem of normal controls and a group of subjects under treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram. 123I-beta-CIT-SPECT was performed in 12 depressed patients under 20 mg (n = 5), 40 mg (n = 6) and 60 mg (n = 1) citalopram daily, in one untreated depressed patient and in 11 controls at regular time intervals up till 24 hours p.inj. A highly significant reduction of beta-CIT binding was found in an area including mesial thalamus, hypothalamus, midbrain and pons in patients under citalopram compared to controls (44.1 +/- 14.4 vs. 82.3 +/- 18.6cpm's/mCi x kg body weight; specific binding 4 hrs p.inj.; p = 0.0001). No differences were seen between the high and low dose group and no changes were found in the striatum. 123I-beta-CIT binding in the brain stem and striatum in one untreated depressed patient fell within the range of control values. To our knowledge this is the first report directly demonstrating the effect of a selective serotonin uptake inhibitor in the brain in humans in vivo. SPECT measurements of serotonin uptake sites in patients with depression and other psychiatric disorders might provide better insights into the pathophysiology of these disorders and into mechanisms of drug action.

Crossed corticothalamic and thalamocortical connections of macaque prefrontal cortex.

We have conducted a systematic comparison of the ipsilateral (uncrossed) and contralateral (crossed) thalamic connections of prefrontal cortex in macaque monkeys, using cortical implants of horseradish peroxidase pellets and tetramethyl benzidine histochemistry to demonstrate anterograde and retrograde thalamic labeling. Contrary to the prevailing belief that thalamocortical projections are entirely uncrossed, our findings indicate that a modest crossed projection to prefrontal cortex arises from the mesial thalamus, principally the anteromedial and midline nuclei. Also, while confirming that corticothalamic projections are bilateral, we found that the pattern of crossed projections differs from that of uncrossed projections. Projections to mesial thalamic nuclei, specifically to the anteromedial nucleus, the midline nuclei, and the magnocellular part of the mediodorsal nucleus are bilateral, the contralateral projection being nearly as dense as the ipsilateral projection. Projections to the parvicellular part of the mediodorsal and ventral anterior nuclei are also bilateral, but the contralateral projection is much weaker than the ipsilateral projection. Prefrontal projections to the reticular nucleus, medial pulvinar, suprageniculate nucleus, and limitans nucleus appear to be exclusively ipsilateral. These results indicate that prefrontal cortex has prominent bilateral and reciprocal connections with the nuclei of the mesial thalamic region. As this region of the diencephalon has been implicated by anatomical and behavioral studies in memory functions, our findings suggest that prefrontal cortex, through its connections with this region, may be involved in the bilateral integration of mnemonic systems.

The role of prefrontal cortex in grand mal convulsion.

In five patients with intractable generalized seizures and nonfocal electroencephalograms, direct brain recordings (from prefrontal and parietal cortices, mesial temporal lobe, and mesial thalamus) were made at rest, during spontaneously occurring seizure, and during pentylenetetrazol induced grand mal convulsion. There was a limited correlation between EEG and records made directly from the brain; generalized atypical spike and wave activity which characterized the interictal EEG emanated from frontal lobes. Mesial thalamus did not show the atypical spike and wave activity seen in pre-frontal cortex; nor could such focal cortical discharge or convulsion be produced by stimulation of mesial thalamus. Both spontaneous and pentylenetetrazol induced grand mal convulsion originated in prefrontal cortex, the thalamus became involved secondarily. The findings together with those extant in current literature indicate an important role for prefrontal cortex in the genesis of both idiopathic and acquired grand mal convulsion.

Effect of stimulation of the human thalamus and parietal and temporal white matter on short-term memory.

C LINICAL and experimental observations 7,~,:'~ indicate that the preservation of memory traces is dependent on specific cerebral mechanisms. Electrical excitation and lesions in the hippocampal formation 1,'-','~,8,2~ and mesial thalamus ~~,~'; have been related to memory deficits in man. Recent evidence 11 has also implicated the ventral lateral thalamus as an anatomic correlate for the storage of memory events. This report describes an attempt to determine whether other lateral thalamic and subcortical structures participate in memory functions. In a previous study 1~ a task of naming and short-term memory for pictorial memoranda was presented to patients with electrodes implanted in the thalamus for treatment of motion disorders. Electrical stimulation in the left pulvinar and deep parietal white substance in both hemispheres disrupted verbal behavior and elicited anomia. The effect of stimulation on the memory performance of these patients with thalamic electrodes and additional patients with temporal lobe electrodes is the subject of this report.