Sensorimotor deficits

Bashki, VP, Swerdlow, NR and Geyer, MA (1994) Clozapine antagonises phencyclidine-induced deficits in sensorimotor gating of the startle response. J. Pharmacol. Exp. Ther. 271 787-794. 

Geyer, MA, Swerdlow, NR, Mansbach, RS and Braff, DL (1990) Startle response models of sensorimotor gating and habituation deficits in schizophrenia. Brain Res. Bull. 25 485-498. 

Children appear to be much more sensitive to lead-related neurobehavioral alterations than adults. Neurobehavioral dysfunction has not been demonstrated in lead-exposed workers at PbB concentrations below 40 pg/dL, whereas cognitive and sensorimotor deficits have been shown in children to be associated with PbB concentrations as low as 10 to 15 pg/dL. To put these findings in perspective, a 1-3 point IQ decrement corresponds to 1/5 or less of a standard deviation of the typical IQ distribution. 

Melatonin receptor (MT1) knockout mice display depression-like behaviors and deficits in sensorimotor gating. Brain Res. Bull. 68, 425-9. 

Abou-Donia, M.B., Dechkovskaia, A.M., Goldstein, L.B., Shah, D.U., Bullman, S.L., and Khan, W.A., Uranyl acetate-induced sensorimotor deficit and increased nitric oxide generation in the central nervous system in rats, Pharmacol. Biochem. Behav., 72, 881-890, 2002. 

The exact nature of the deficit produced by NMDA antagonists and the interpretation of results has been questioned. It is difficult to ignore the possibility that sensorimotor impairment, however subtle, may mediate the apparent spatial learning deficit in rats (Keith and Rudy, 1990). The fact that animals exhibiting minimal LTP still demonstrate significant learning is also challenging (Bannerman et al., 1995). 

Neurobehavioral examinations are useful for identifying neurotoxicant-mediated deficits, but it is often difficult to localize the site of toxic action from such tests. For example, sensorimotor tests of reaction time, manual dexterity, hand-eye coordination, and finger tapping can indicate either neuromuscular or psychomotor damage. 

Geyer MA, Krebs-Thomson K, Braff DL, Swerdlow NR. Pharmacological studies of prepulse inhibition models of sensorimotor gating deficits in schizophrenia a decade in review. Psychopharmacology 2001 156 117-154. 

Feifel D, Melendez G, Shilling PD. Reversal of sensorimotor gating deficits in Brattleboro rats by acute administration of clozapine and a neurotensin agonist, but not haloperidol a potential predictive model for novel antipsychotic effects. Neuropsychopharmacology 2004 29 731-738. 

Sensorimotor deficits imitating peripheral nerve involvement were reported (Back and Mrowka 2001). Ulnar and median nerve-like deficit were due to infarcts located in the thalamus and the corona radiate (Lampl et al. 1995). We have seen two patients with radial nerve-like deficits due to cortical ischemic lesions of the cortical presentation of the hand in the motor cortex. Normal nerve conduction velocity and MRI help to clarify these cases. 

Gould TJ, Bizily SP, Tokarczyk J, Kelly MP, Siegel SJ, et al. 2004. Sensorimotor gating deficits in transgenic mice expressing a constitutively active form of Gs alpha. Neuropsychopharmacology 29 494-501. 

Braff DL, Geyer MA, Light GA, Sprock J, Perry W, Cadenhead KS, Swerdlow NR (2001) Impact of prepulse characteristics on the detection of sensorimotor gating deficits in schizophrenia. Schizophr Res 49 171-178. 

Dunnett SB, Lane DM, Winn P (1985) Ibotenic acid lesions of the lateral hypothalamus comparison with 6-hydroxydopamine induced sensorimotor deficits. Neuroscience 74 509-518. 

Mandel RJ, Brundin P, Bjorklund A (1990) The importance of graft placement and task complexity for transplant induced recovery of simple and complex sensorimotor deficits in dopamine denervated rats. Eur J Neurosci 2 888-894. 

Schallert T, Hall S (1988) Disengage sensorimotor deficit following apparent recovery from unilateral dopamine depletion. Behav Brain Res 20 15-24. 

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. 

Neurofilament and peripherin mutations were reported in rare forms of ALS (Gros-Louis et al., 2004 Leung et at., 2004), leading researchers to develop animal models bearing these mutations (Millecamps et al., 2006). Although these mice developed no evident MND, some exhibited moderate sensorimotor and spatial deficits probably due to the observed reduction in conduction velocity. 

Abou-Donia et al, 2002). Intramuscular injection of 0.1 and 1.0 mg/kg for 7 days, followed by a 30-day observational period, resulted in sensorimotor deficits in rat behavior, differential levels of NO, and increased acetylcholinesterase activity in the cortex of animals dosed with 1 mg/kg, suggesting multiple exposures to low doses of uranyl acetate caused prolonged neurobehavioral deficits in rats after the initial exposure has ceased, similar to the exposures of Gulf War veterans (Abou-Donia et al, 2002). 

Like the pharmacological model presented above, a genetic model also targets the NMDA receptor. This model was created by knocking down the NRl subunit of the NMDA receptor, which is obligatory for receptor function, in mice so that only 5% of the protein is expressed (117). These animals, also known as NRl hypomorphs, show NMDA receptor hypofunc-tion and display several schizophrenia-like behaviors, such as reduced social interactions, increased locomotion, stereotypic movements, and sensorimotor gating deficits (117, 118). Interestingly, treatment of these mice with the atypical antipsychotic... 

Duncan GE, Moy SS, Perez A, Eiddy DM, Zinzow WM, Lieber-man JA, Snouwaert JN, Roller BH Deficits in sensorimotor gating and tests of social behavior in a genetic model of reduced NMDA receptor function. Behav. Brain Res. 2004 153 507-19. 

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