Brain-stem

CJ-Receptors are localized ia the brain stem and limbic stmcture, regions associated with endocrine function (76). In the periphery, CJ-receptors are found in the Hver, heart, ileum, vas deferens, and on lymphocytes and thymocytes. Although there is insufficient evidence to clearly define the functional role of CNS CJ-sites, based on the effects of PCP and the interaction of haloperidol with CJ-sites, CJ-receptor ligands may be antipsychotics or used for the treatment of substance abuse. Several CJ-receptor ligands have shown neuroprotective effects in vivo. Ifenprodil (315) and CNS 1102 (316) are being developed for treatment of stroke (Table 18). 

OT receptors are localized ia the brain hypothalamus, limbic system, cortex, striatum, olfactory system, and brain stem. In the periphery, OT is best known for its stimulation of uterine smooth muscle and the milk ejection reflex. Thr , Om ]oxytocin(l—8),... 

The chromaffin cells of the adrenal medulla may be considered to be modified sympathetic neurons that are able to synthesize E from NE by /V-methylation. In this case the amine is Hberated into the circulation, where it exerts effects similar to those of NE in addition, E exhibits effects different from those of NE, such as relaxation of lung muscle (hence its use in asthma). Small amounts of E are also found in the central nervous system, particularly in the brain stem where it may be involved in blood pressure regulation. DA, the precursor of NE, has biological activity in peripheral tissues such as the kidney, and serves as a neurotransmitter in several important pathways in the brain (1,2). 

Arousal is a state of vigilance regulated by subcortical parts of the nervous system, especially connections between the nuclei of the amygdala, the hypothalamus and the brain stem. These unconscious responses prepare the body for action. 

Dementia with Lewy bodies (DLB) is considered the second most common cause of dementia after AD. The disorder is characterized by progressive fluctuating cognitive impairment, visual hallucinations and motor features of Parkinsonism. Neocoitical cholinergic activity is more severely depleted in DLB than in AD, and DLB also affects the caudate nucleus, the thalamus and the brain stem. Tolerability of ChEI in DLB appears similar to AD, with some gastrointestinal effects and muscle cramps. 

Thored P, Arvidsson A, Cacd E, Ahlenius H, KaUur T, Darsaha V, Ekdahl CT, Kokaia Z, LindvaU O (2006) Persistent production of neurons from adult brain stem cells during recovery after stroke. Stem Cells 24 739-747... 

Tetanus occurs when Cl. tetani, ubiquitous in the soil and faeces, contaminates wounds, especially deep puncture-type lesions. These might be minor traumas such as a splinter, or major ones such as battle injury. At these sites, tissue necrosis and possibly microbial growth reduce the oxygen tension to allow this anaerobe to multiply. Its growth is accompanied by the production of a highly potent toxin which passes up peripheral nerves and diSuses locally within the central nervous system. It acts like strychnine by affecting normal function at the synapses. Since the motor nerves of the brain stem are the shortest, the cranial nerves are the first affected, with twitches of the eyes and spasms of the jaw (lockjaw). 

Acute exposure to trichloroethylene and its decomposition products (e.g., dichloroacetylene) has also led to residual neuropathy, characterized by nerve damage. This neuropathy is characterized by facial numbness, jaw weakness, and facial discomfort (indicating damage to cranial nerves V and VII) which can persist for several months (Buxton and Hayward 1967 Feldman 1970). Chronic exposure in the workplace has also been associated with damage to the cranial nerves in several cases (Bardodej and Vyskocil 1956 Barret et al. 1987 Cavanagh and Buxton 1989). Persons who have died from overexposure have shown degeneration of cranial nuclei in the brain stem (Buxton and Hayward 1967). Some of these effects may be attributed to... 

O Brien, JA and Berger, AJ (1999) Cotransmission of GABA and glycine to brain stem motoneurons. J. Neurophysiol. 82 1638-1641. 

Fuxe 1965) and throughout the brain stem and spinal cord. A series of studies employing small intracerebral lesions (Anden et al. 1966 Ungerstedt 1971) indicated that most 5-HT nerve terminals in the forebrain arise from raphe nuclei in the midbrain and that the axons ascend through the lateral hypothalamus within the medial forebrain bundle (Moore and Heller 1967 Azmitia 1978 Conrad et al. 1974). 

Taber, E. Brodal, A. and Walberg. F. The raphe nuclei of the brain stem in the cat. I. Normal topography and cytoarchitecture and general discussion. J Comp Neurol 114 161-187, 1960. 

Wiklund, L. Leger, L. and Persson, M. Monoamine cell distribution in the cat brain stem. A fluorescence histochemical study with quantification of indolaminergic and locus coeruleus cell groups. J Comp Neurol 203 613-647, 1981. 

Fig. 2.20 Efferent pathways into bulb showing (a) cholinergic (ACh) fibres projecting to MOB from basal forebrain nuclei. AON = ant. olfactory nucleus, OT = olfactory tract, DB = diagonal band nuc. (from Davis et al., 1978). (b) Nor-Adrenalin input to AOB, via MFB pathway from brain stem centres (nuclei A1-2, A6) (from Keveme, 1971).

Benzodiazepines, especially lorazepam, are used to prevent and treat CINV.5,10 Lorazepam is thought to prevent input from the cerebral cortex and limbic system from reaching the central vomiting center in the brain stem.10 Sedation and amnesia are common side effects. Respiratory depression can occur with high doses or when other central depressants such as alcohol are combined with benzodiazepines. 

The extrapyramidal motor system controls muscle movement through a system of pathways and nerve tracts that connect the cerebral cortex, basal ganglia, thalamus, cerebellum, reticular formation, and spinal neurons. Patients with PD lose dopamine neurons in the substantia nigra, which is located in the midbrain within the brain stem. The substantia... 

The triptans are considered specific therapies in that they target the pathophysiology underlying migraine.33 They abort headache through beneficial effects on neuronal imbalances.11 Triptans inhibit neurotransmission in the trigeminal complex and activate serotonin lb/Id pathways that modulate nociception in the brain stem. They also decrease the release of vasoactive peptides leading to vascular reactivity and pain.34 Triptans are a welcome addition to the therapeutic armamentarium in that they are available in intranasal, subcutaneous, and oral... 

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