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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. 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. This article highlights the common observation of acute hyporeflexia after central nervous system insults and explores the underlying anatomy and physiology.
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. 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, the proposed connectivity can be generalized to help explain other insults including stroke, atonic seizures, and spinal shock. 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.
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. This observation may yield insight into functional connectivity underlying pathological spinal reflexes. SMA syndrome has been described most commonly as a result of surgical resection of cortex anterior to the precentral gyrus Laplane et al.
Classically, it follows a triphasic pattern, with an initial contralateral akinesia lasting several days that is often associated with preserved strength for involuntary movements. This is followed by a reduction in spontaneous activity of the contralateral limbs that lasts for days to weeks.
If the dominant speech hemisphere is involved, then the early phase is also associated with expressive aphasia. It is worth emphasizing that the syndrome that follows resection of the SMA includes hemiparesis usually without hyperreflexia, and typically acute hyporeflexia is seen in this syndrome despite the unequivocal preservation of the primary motor cortex and its contributions to the corticospinal tract Krainik et al.
Although the SMA has extensive projections through the motor systems, a key observation to derive an explanation for these classically LMN findings is that direct cortical stimulation of the primary motor cortex does not always cause motor movements immediately after the SMA syndrome occurs.
This has been observed intra-operatively by the authors and described by others with motor evoked potentials following SMA resection Zentner et al. Understanding this finding of blocked transmission from primary motor cortex neurons that end on alpha motor neurons of the spinal cord augments historic descriptions of the connectivity. With intact corticospinal tracts from the motor cortex, the lost response to cortical stimulation along with hyporeflexia appears consistent with more distal interruption, perhaps at the level of the spinal cord, caused by the loss of the SMA contribution to the corticospinal tract.
This observation has been difficult to reconcile with conceptions of the anatomico-functional relationship between the SMA, primary motor cortex, and the spinal cord. In this article, we review historic explanation for the acute hyporeflexia of UMN injuries and propose a theory implicating corticospinal tracts originating outside of the primary motor cortex. We hypothesize that the SMA contributions to the motor system provide a net inhibitory influence on the spinal cord and acute compromise is a dominant effector of acute hypotonia and hyporeflexia.
Clinical Insights Spinal shock offers the classically described paradigm of acute hypotonic plegia after CNS injury. Over the last two centuries, the teaching that has persisted is that this hyporeflexia is caused by loss of excitatory background descending input to the spinal motor neurons and interneurons leading to a hyperpolarization Ashby et al.
However, lost descending tonic influence is also used to explain the increased excitability that is associated with delayed spinal cord injury Nielsen et al.
Further, it is accepted that alpha motor neuron depression is not the sole source for reflex depression Hiersemenzel et al.
Other contributory metabolic, humoral, and structural mechanisms have been proposed to explain the temporal evolution of spinal shock to eventual hypertonicity and hyperreflexia, but they fail to clearly explain the initial reflex response and have clouded our interpretation of UMN function Hiersemenzel et al.
Even focal and incomplete injuries to the spinal cord, in anterior spinal artery infarct, for example, are similarly associated with an initial flaccid weakness Suzuki et al. In a complementary manner, the reflex recovery after supplementary motor cortex resection occurs over days to weeks as is expected after acute spinal cord injury Dittuno and Ditunno, ; Krainik et al.
Spinal Reflex Arc A reflex conveys an afferent stimulus to an effector via an integration center, and a simple physiologic version is the monosynaptic arc that underlies the deep tendon reflex Figure 1.
The responsiveness of the two neuron backbone is the result of an interplay between the local segmental inputs and descending influences.
The context of reflex responsiveness is often key to interpreting their significance, and the physiology at play is not always evident. UMN lesions are said to result in a net loss of inhibition that enhances tonic and phasic stretch reflex responses Brashear and Elovic, , however, this is not always clinically observed.
This figure illustrates the classically described spinal reflex arc and the historically described contradictory changes in output resulting from corticospinal tract injury. Arrows indicate the increased alpha motor neuron output as a result of injury to the corticospinal tract, despite the direct connection and stimulatory output from the motor cortex.
The extensive synaptic contributions to the monosynaptic tendon reflex complex are illustrated by exploring the afferent and efferent connectivity of the alpha motor neuron Figure 2. Supraspinal input includes the corticospinal tract, the rubrospinal tract, the vestibulospinal tract; and segmental and intersegmental input includes the interneuron pool and extensive sensory afferents Carpenter, ; Kingsley et al. There is a non-linearity to the input-output relationship of the motor neuronal pool, and the influence of some neuronal inputs may not be sufficient to independently achieve an excitation threshold but other neurons can facilitate Emmanuel Pierrot-Deseilligny, Conversely, the postsynaptic output following simultaneous stimulation by two input neurons can be less than that following stimulation by only one of the neurons, a phenomenon called occlusion.
As the interneurons play a large role in the ultimate response of the alpha motor neurons, afferent, and efferent contributions to this neuron pool may be consequential in the response to injury. While the nature of these interactions is not entirely understood for all contributors, it is clear that alpha motor neuron stimulation and suppression is achieved via a complex and poorly quantified afferent pool that influences the central state of the cells.
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