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Biomedical subjects

Michael S Salman

Publications and source records attributed to Michael S Salman.

9 recordsLinked to original sources
PubMed2006

Saccadic adaptation in Chiari type II malformation.

BACKGROUND: Saccadic adaptation corrects errors in saccadic amplitude. Experimentally-induced saccadic adaptation provides a method for studying motor learning. The cerebellum is a major participant in saccadic adaptation. Chiari type II malformation (CII) is a developmental deformity of the cerebellum and brainstem that is associated with spina bifida. We investigated the effects of CII on saccadic adaptation. METHOD: We measured eye movements using an infrared eye tracker in 21 subjects with CII (CII group) and 39 typically developing children (control group), aged 8-19 years. Saccadic adaptation was induced experimentally using targets that stepped horizontally 120 to the right and then stepped backward 3 degrees during saccades. RESULTS: Saccadic adaptation was achieved at the end of the adaptation phase in participants in each group. Saccadic amplitude gain decreased by 6.9% in the CII group and 9.3% in the control group. The groups did not differ significantly (p = 0.27). Amplitude gain reduction was significantly less in the CII participants who had multiple shunt revisions. Regression analyses revealed no effects of spinal lesion level, presence of nystagmus, or cerebellar vermis dysmorphology on saccadic adaptation. CONCLUSION: The neural circuits involved in saccadic adaptation appear to be functionally intact in CII.

Adaptation, Physiological↗
PubMed2006

Saccadic adaptation in children.

Saccades are fast-orienting eye movements. Saccadic adaptation, a form of motor learning, is a corrective change in the amplitude of saccades in response to error. The aim of the study was to ascertain whether saccadic adaptation occurs in typically developing children. We recorded saccades with an infrared eye tracker in 39 children, aged 8 to 19 years, at baseline to 12-degree horizontal target steps and after an adaptive task. During the adaptive task, a saccadic hypometric error was induced. This task consisted of 200 12-degree target steps that stepped backward 3 degrees during the initial saccade and without the participants' awareness. The initial saccade triggered the back-step. This paradigm required a corrective reduction of the amplitude of the initial saccades in response to the induced error. Saccadic adaptation was achieved in 26 participants, whose mean saccadic amplitudes decreased by 13% (P < .05). Saccadic adaptation was not influenced by age. We conclude that children as young as 8 years old have established functions of the neural circuits responsible for the motor learning required for saccadic adaptation.

Adaptation, Physiological↗
PubMed2005

Cerebellar vermis morphology in children with spina bifida and Chiari type II malformation.

OBJECTIVE: Posterior fossa size and cerebellar weight and volume are reduced in Chiari type II malformation (CII). This is assumed to affect the cerebellum uniformly. We quantified the presumed reduction in vermis size on magnetic resonance imaging (MRI). METHODS: A midsagittal brain MRI slice was selected from each of 68 participants with CII (mean age 13 years). Control participants were 28 typically developing children (mean age 14.1 years). Midsagittal surface areas occupied by the intracranial fossa, posterior fossa, vermis, and its lobules were measured. CONCLUSIONS: Mean posterior fossa area was significantly smaller (P<0.003), although mean vermis area was significantly larger (P<0.0001), in participants with CII than in control participants. This expansion involved vermis lobules I-V and VI-VII areas (P<0.0001). The midsagittal vermis was expanded and not reduced in size in participants with CII. This is attributed to compressive displacement of midline structures within the confines of a small posterior fossa.

Adolescent↗
PubMed2005

Smooth pursuit eye movements in children.

Smooth pursuit eye movements consists of slow eye movements that approximate the velocity of the eyes to that of a small moving target, so that target image is kept at or near the fovea. Little information on smooth pursuit is available in children. We used an infrared eye tracker to record smooth pursuit in 38 typically developing children, aged 8-19 years. Participants followed a visual target moving sinusoidally at +/-10 degrees amplitude, horizontally and vertically at 0.25 or 0.5 Hz. The mean horizontal smooth pursuit gains, the ratio of eye to target velocities, were 0.84 at 0.25 Hz and 0.73 at 0.5 Hz. Mean vertical smooth pursuit gains were 0.68 at 0.25 Hz and 0.45 at 0.5 Hz. Smooth pursuit gains were significantly lower for vertical in comparison to horizontal tracking, and for 0.5 Hz in comparison to 0.25 Hz tracking (P<0.0001). Smooth pursuit gains increased with age (P<0.01, Pearson's correlation tests), with horizontal gains attaining reported adult values by mid adolescence. Vertical gains had large variability among participants. The median phase, the time interval between eye and target velocities, varied between 39 and 86 ms. Phase was not influenced by age. We conclude that smooth pursuit gains are lower in children than gains reported in adults. Vertical pursuit gain is significantly lower than horizontal pursuit gain. Gains improve with age and approach adult values in mid adolescence. Children have larger phases than reported adults values indicating that prediction in the smooth pursuit system is less mature in children.

Adolescent↗
PubMed2005

Saccades in children.

Saccades are necessary for optimal vision. Little is known about saccades in children. We recorded saccades using an infrared eye tracker in 39 children, aged 8-19 years. Participants made saccades to visual targets that stepped 10 degrees or 15 degrees horizontally and 5 degrees or 10 degrees vertically at unpredictable time intervals. Saccadic latency decreased significantly with increasing age, while saccadic gain and peak velocity did not vary with age. Saccadic gains and peak velocities in children are similar to reported adult values. This implies maturity of the neural circuits responsible for making saccades accurate and fast. Saccade latency decreases as the brain matures.

Adolescent↗
PubMed2003

Pontocerebellar hypoplasia type 1: new leads for an earlier diagnosis.

Pontocerebellar hypoplasia type 1 is a rare disease characterized by pontocerebellar hypoplasia and anterior horn cell degeneration. The oldest reported child died at the age of 26 months. Two siblings were diagnosed with pontocerebellar hypoplasia type 1 after the death of the second sibling at 40 months of age from respiratory failure and the unexpected finding of anterior horn cell degeneration on her autopsy. The older sibling was a boy who was labeled as having cerebral palsy. He died at 14 months of age from pneumonia following a clinical course similar to his sister's, who was born 5 years after his death. Both siblings had significant global developmental delay with axial and peripheral hypotonia initially. Peripheral hypertonia with brisk reflexes developed later but were absent prior to death. Extensive investigations in the second sibling ruled out known metabolic (including congenital disorders of glycosylation) and mitochondrial diseases using skin fibroblast cultures and enzyme analysis. Genetic testing for Friedreich's ataxia; neuropathy, ataxia, and retinitis pigmentosa (NARP); spinal muscular atrophy; and spinocerebellar ataxia type 1, 2, 3, 6, 7, and 8 gene abnormalities was negative. The elecroretinogram showed a previously unreported finding of abnormal and progressive rod/cone response. Our cases provide clinical and previously unreported electroretinographic evidence for neurodegeneration in pontocerebellar hypoplasia type 1 and call for the expansion of the disease phenotype.

Atrophy↗
PubMed2002

New insights into the neuropathogenesis of molybdenum cofactor deficiency.

BACKGROUND: Molybdenum cofactor deficiency (MOCOD) is a rare, progressive neurodegenerative disorder caused by sulphite oxidase enzyme deficiency. The neuropathological findings are consistent with a toxic insult to the brain that causes severe neuronal loss, reactive astrogliosis and spongiosis. The mechanisms responsible for these changes are unknown. METHODS: The case is a male infant with MOCOD who died at nine months of age from pneumonia. At autopsy, a complete neuropathological examination was performed including conventional immunohistochemical staining. In addition, brain sections were stained cytochemically with shikata and orcein which stain for disulphide bonds. The elemental composition of cortical cells was then analyzed in the scanning electron microscope using backscatter electron imaging and energy dispersive X-ray spectrometry. RESULTS: Neurons demonstrated cytoplasmic staining with shikata and orcein cytochemically when compared to control sections. Energy dispersive X-ray spectrometry analysis of these neurons confirmed the presence of excess sulphur and unexpectedly revealed excess magnesium accumulation. None of these findings was found in an age-matched control. CONCLUSIONS: In MOCOD we found abnormal accumulation of sulphur and magnesium in neurons. It is postulated that sulphur-containing compound(s) that are formed as a result of MOCOD cause excitotoxic neuronal injury in the presence of excess magnesium.

Autopsy↗
PubMed2002

The cerebellum: it's about time! But timing is not everything--new insights into the role of the cerebellum in timing motor and cognitive tasks.

Converging evidence from different research studies supports a role for the cerebellum in timing neural processes. The cerebellum is part of a distributed system for motor control. The timing hypothesis provides a specific functional role for the unique contribution of the cerebellum. The timing capabilities of the cerebellum appear to extend beyond motor control into tasks focusing on perceptual processing that require the precise representation of temporal information and sensorimotor learning. Behavioral and modeling studies suggest that the cerebellar timing system is best characterized as providing a near-infinite set of interval-type timers rather than as a single clock with pacemaker or oscillatory properties, but this is controversial. In addition to learning precisely timed motor responses, the cerebellum is involved in on-line processing using feed-forward systems for which sensory input is used prior to movement execution to improve movement accuracy. This would be a mechanism for triggering accurate "time." The cerebellum continues to fascinate scientists, and although survival is possible without the cerebellum, the resultant quality of life is significantly compromised with clumsiness, ataxia, hypotonia, dysarthria, slowing of various cognitive perceptual processes, and impaired fine motor and ocular-motor coordination. The last three decades have seen the development of research that has focused on how the cerebellum functions. Further neurophysiologic research in cerebellar cortical neurotransmission is likely to further our understanding of the cerebellar contribution to timing sensorimotor processes.

Animals↗