Lesion thalamic

The slow (deep sleep) -waves probably originate in the eortex beeause they survive separation from, or lesions of, the thalamus. However, the rhythm and appearanee of spindles in earlier phases of the sleep eyele do depend on links with the thalamus (see Steriade 1999). Unlike stimulation of the specific sensory relay nuclei in the thalamus, which only affects neurons in the appropriate sensory areas of the cortex, the nonspecific nuclei can produce responses throughout the cortex and may not only control, but also generate, cortical activity. Certainly, in vitro studies show that neurons of the non-specific reticular thalamic nucleus (NspRTN) can fire spontaneously at about 8-12 Hz (equivalent to EEG a-rhythm) or lower, and that low-frequency stimulation of this area can induce sleep. 

Administration of HA and its effect on sleep-wakefulness Local application of HA (5, 30 and 60 pg) in the TMN region of cats increased the latency to sleep, increased arousal, and reduced NREM sleep in a site-specific, dose-dependent manner. The highest dose produced the maximal effect, which lasted for 6 h. The HA-induced arousal was completely blocked when the cats were pretreated intraperitoneally with the Hi receptor antagonist mepyramine (Lin et at, 1986, 1988). In rats, intraventricular administration of HA blocked the increase in delta and theta activity (0-6 Hz) in the EEG induced by repeated low-frequency stimulation of the midbrain reticular formation. This effect was blocked if specific thalamic nuclei were lesioned (Tasaka et at, 1993) or by simultaneous administration of an Hi receptor antagonist, but not by an H2 receptor antagonist (Tasaka et at, 1989). Application of HA... 

Ferreira, A., Dahlof, L. G., and Hansen, S. (1987). Olfactory mechanisms in the control of maternal aggression, appetite, and fearfulness effects of lesions to olfactory receptors, mediodorsal thalamic nucleus, and insular prefrontal cortex. Behavioral Neuroscience 101, 709-717. 

The contention that the thalamocortical system is essential to the synchronous activation of the forebrain and hence to consciousness is supported by the loss of consciousness in subjects with disease destruction of the thalamus and by the capacity to restore consciousness by activating the thalamocortical system if that system (and of course, the cortex) is intact. The case of Karen Ann Quinlan is well known her profound coma was caused by a very small, restricted thalamic lesion and was irreversible because the thalamocortical system could not be activated by any known means. 

Kuker et al. (2002) 45 Clinical symptoms of akute infratentorial or thalamic infarction Sensivity of DWI and T2 is lower earlier than 12 h after onset and for medulla-oblongata lesions... 

Acute or chronic cerebral injury may cause effects in remote areas of brain (Meyer et at 1993), so-called diaschisis, by reducing neuronal inputs and metabolic activity in the contralateral cerebellum and ipsilateral internal capsule, thalamus and basal ganglia after cortical lesions in the ipsilateral cortex following internal capsule and thalamic lesions and in the contralateral hemisphere. The functional consequences of diaschisis are not clear (Bowler et at 1995). 

Small thalamic lesions may cause a pure sensory stroke or sensorimotor stroke, sometimes with ataxia in the same limbs (Schmahmann 2003). However, other deficits may occur in isolation, or in combination depending on which thalamic nuclei are involved. These include paralysis of upward gaze, small pupils, apathy, depressed consciousness, hypersomnolence, disorientation, visual hallucinations, aphasia and impairment of verbal memory attributable to the left thalamus, and visuospatial dysfunction attributable to the right thalamus. Occlusion of a single small branch of the proximal posterior cerebral artery can cause bilateral paramedian thalamic infarction with severe retrograde and anterograde amnesia. 

Post-stroke, or thalamic, pain is a burning, severe and paroxysmal pain exacerbated by touch and other stimuli. Such post-stroke pain is rare and usually occurs weeks or months after stroke (Nasreddine and Saver 1997 Frese et al. 2006). There are usually some sensory signs in the affected areas. The lesion is usually located in the contralateral thalamus but may lie elsewhere in the central sensory pathways. Treatment includes anticonvulsants, amitriptyline and various sorts of counter-stimulation but is often unsuccessful. 

Hugdahl K, Wester K, Asbjpmsen A (1991, Oct) Auditory neglect after right frontal lobe and right pulvinar thalamic lesions. Brain Lang 41(3) 465 73 Hutton M, Perez-Tur J, Hardy J (1998) Genetics of Alzheimer s disease. Essays Biochem 33 117-131... 

Sorensen JC, Dalmau I, Zimmer J, Finsen B (1996) Microglial reactions to retrograde degeneration of tracer-identified thalamic neurons after frontal sensorimotor cortex lesions in adult rats. Exp Brain Res 112 203—212. 

In fhe case of patienfs, fhe only reporf in which the authors claim that star fruit intoxication induce brain lesions (in this case thalamic and cortical) is the one from Chan YL ef al [11]. Unfortimafely fhere is no neurological follow up of fhe evenfual neurological sequelae thaf patienfs who survive will display in fheir future hves after the treatment s rescue. 

The concept of schizophrenia as a neurode- velopmental disorder has inspired attempts to create adverse and early postnatal events in, animals to model the psychopathological processes underlying the disorder (109, 110). These neurodevelopmental models include prenatal malnutrition, viral infection and hypoxia, disrupted neurogenesis by X-ray irradiation or neurotoxins in utero, adverse postnatal experiential factors such as maternal deprivation and social isolation, and postnatal brain damage created by hippocampal, neocor-tical, or thalamic lesions (109-111). With the possible exception of maternal deprivation and social isolation, these models have not been sufficiently characterized pharmacologically to be used for antipsychotic drug screening. 

Sabin M, Bowen WD, Donoghue JP. 1992. Location of nicotinic and muscarinic cholinergic and mu-opiate receptors in rat cerebral neocortex Evidence from thalamic and cortical lesions. Brain Res 579 135-147. 

The most effective surgical technique is deep brain stimulation (DBS) of the STN, which decreases outflow from this region (as shown in Fig. 57-2S) and thus reduces input to the thalamus. STN DBS is especially useful for tremor, dyskinesias, gait disorder, and start hesitation. Thalamic DBS and thalamotomy (a focal destructive lesion of the thalamus) can reduce disabling tremor. Pallidotomy (a focal destructive lesion of the GPi) and GPi DBS can help with severe dyskinesias and on/off fluctuations but is not as helpful for bradykinesia. Destructive lesions are immediate and permanent, whereas DBS requires lifelong maintenance. Transplantation of autologous adrenal medulla tissue was unsuccessful, as has been more recent experience in most cases of fetal tissue transplantation. 

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