![]() ![]() This observation may yield insight into functional connectivity underlying pathological spinal reflexes. However, hyporeflexia, atonia, and other lower motor neuron (LMN) signs are observed after acute central nervous system insults such as SMA syndrome and spinal shock. These “release signs” were described by Hughlings Jackson in 1931 as “positive signs” ( Jackson et al., 1931), and have been suggested to be enhanced reflexes released by pyramidal lesions ( Landau and Clare, 1959). Hyperreflexia and hypertonia are the classic upper motor neuron (UMN) signs thought to occur from the loss of corticospinal motor tract suppression of the spinal reflex arc. Further, the proposed connectivity can be generalized to help explain other insults including stroke, atonic seizures, and spinal shock. Unlike traditional explanations, this theory more adequately explains the findings of postoperative supplementary motor area syndrome in which hyporeflexia motor deficit is observed acutely in the face of intact primary motor cortex connections to the spinal cord. Further, evidence for the underlying connectivity is presented and implicates the dominant role of supraspinal inhibitory influence originating in the supplementary motor area descending through the corticospinal tracts. This article highlights the common observation of acute hyporeflexia after central nervous system insults and explores the underlying anatomy and physiology. Unfortunately, these simple descriptions consistently fail to adequately explain the pathophysiology and connectivity leading to acute hyporeflexia and delayed hyperreflexia that result from such insult. Historic theories to explain these contradictory findings have implicated a number of potential mechanisms mostly relying on the loss of descending corticospinal input as the underlying etiology. ![]() However, acute hypotonia and areflexia with motor deficit are hallmark findings after many central nervous system insults such as acute stroke and spinal shock. Hypertonia and hyperreflexia are classically described responses to upper motor neuron injury. 3Division of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada.2Department of Neurosurgery, Gui de Chauliac Hospital, Montpellier University Medical Center, Montpellier, France.1Neurosciences Institute, Maine Medical Center, Portland, ME, USA.The weak link: Hypotonia in infancy and autism early identification. A child with self-improving hypotonia: Look at the skin! (20)30695-8/fulltext You can learn more about how we ensure our content is accurate and current by reading our editorial policy. ![]() We link primary sources - including studies, scientific references, and statistics - within each article and also list them in the resources section at the bottom of our articles. Medical News Today has strict sourcing guidelines and draws only from peer-reviewed studies, academic research institutions, and medical journals and associations. This form of hypotonia does not usually progress, tends to improve with treatment, and may run in families. If screenings and tests do not yield clear results, physicians may eventually diagnose children with benign congenital hypotonia, or BCH.
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