Sensory sequelae of medullary infarction: differences between lateral and medial medullary syndrome.
BACKGROUND AND PURPOSE: A comparison between long-term sensory sequelae of lateral medullary infarction (LMI) and medial medullary infarction (MMI) has never been made. METHODS: We studied 55 patients with medullary infarction (41 with LMI and 14 with MMI) who were followed up for >6 months. We examined and interviewed the patients with the use of a structured format regarding the most important complaints, functional disabilities, and the presence of sensory symptoms. The nature and the intensity of sensory symptoms were assessed with the modified McGill-Melzack Pain Questionnaire and the visual analog scale, respectively. RESULTS: There were 43 men and 12 women, with an average age of 59 years. Mean follow-up period was 21 months. The sensory symptoms were the most important residual sequelae in LMI patients and the second most important in MMI patients. In LMI patients, the severity of residual sensory symptoms was significantly related to the initial severity of objective sensory deficits (P<0.05). Sensory symptoms were most often described by LMI patients as numbness (39%), burning (35%), and cold (22%) in the face, and cold (38%), numbness (29%), and burning (27%) in the body/limbs, whereas they were described as numbness (60%), squeezing (30%) and cold (10%), but never as burning, in their body/limbs by MMI patients. LMI patients significantly (P<0.05) more often cited a cold environment as an aggravating factor for the sensory symptoms than did the MMI patients without spinothalamic sensory impairment. The subjective sensory symptoms were frequently of a delayed onset (up to 6 months) in LMI patients, whereas they usually started immediately after the onset in MMI patients. CONCLUSIONS: Our study shows that sensory symptoms are major sequelae in both LMI and MMI patients. However, the nature, the mode of onset, and aggravating factors are different between the 2 groups, which probably is related to a selective involvement of the spinothalamic tract by the former and the medial lemniscus by the latter. We suggest that the mechanisms for the central poststroke pain or paresthesia may differ according to the site of damages on the sensory tracts (spinothalamic tract versus medial lemniscal tract). (+info)
Peripheral demyelination and neuropathic pain behavior in periaxin-deficient mice.
The Prx gene in Schwann cells encodes L- and S-periaxin, two abundant PDZ domain proteins thought to have a role in the stabilization of myelin in the peripheral nervous system (PNS). Mice lacking a functional Prx gene assemble compact PNS myelin. However, the sheath is unstable, leading to demyelination and reflex behaviors that are associated with the painful conditions caused by peripheral nerve damage. Older Prx-/- animals display extensive peripheral demyelination and a severe clinical phenotype with mechanical allodynia and thermal hyperalgesia, which can be reversed by intrathecal administration of a selective NMDA receptor antagonist We conclude that the periaxins play an essential role in stabilizing the Schwann cell-axon unit and that the periaxin-deficient mouse will be an important model for studying neuropathic pain in late onset demyelinating disease. (+info)
Investigation of the functional correlates of reorganization within the human somatosensory cortex.
Much work in animals and humans has demonstrated the existence of changes in topographic organization within the somatosensory cortex (SSC) after amputation or nerve injury. Afferent inputs from one area of skin are able to activate novel areas of cortex after amputation of an adjacent body part. We have investigated the functional consequences of this reorganization in a group of patients with nerve injury. Using the microneurographic technique of intraneural microstimulation (INMS) we stimulated groups of nerve fibres, within individual fascicles proximal to the nerve transection, with small electrical pulses. This enabled us to activate the deafferented cortex that had presumably undergone remodelling and study the conscious percepts described by the subjects. In 39 fascicles from 10 subjects, we found that the sensations evoked on INMS were no different from those reported previously by subjects with intact nerves. This finding suggests that such reorganization within the SSC has little effect on the function of deafferented cortical neurones or subcortical relay stations. In a separate set of experiments, INMS was performed in 16 nerve fascicles from an adjacent non-injured nerve or uninjured fascicle within a partially injured nerve. The sensations evoked by INMS in these experiments were also comparable to those obtained in normal subjects. This indicates that the expanded cortical representation of adjacent non-anaesthetic skin does not influence the cortical processing of afferent information. Taken together, these findings lead us to question the notion that reorganization of connections within the somatosensory cortex equates to a change in function. Whilst it may be advantageous that the human brain is not 'hard-wired', neurophysiological proof of functional plasticity in the adult somatosensory system as a result of deafferentation is elusive. (+info)
Lower lip numbness due to peri-radicular dental infection.
Lower lip numbness has always been a sinister symptom. Much has been written about it being the sole symptom of pathological lesions and metastatic tumours in the mandible. It may also be a symptom of manifestations of certain systemic disorders. A case of lower lip numbness resulting from the compression of the mental nerve by a peri-radicular abscess is presented because of the unusual nature of this spread of infection. (+info)
Left tactile extinction following visual stimulation of a rubber hand.
In close analogy with neurophysiological findings in monkeys, neuropsychological studies have shown that the human brain constructs visual maps of space surrounding different body parts. In right-brain-damaged patients with tactile extinction, the existence of a visual peripersonal space centred on the hand has been demonstrated by showing that cross-modal visual-tactile extinction is segregated mainly in the space near the hand. That is, tactile stimuli on the contralesional hand are extinguished more consistently by visual stimuli presented near the ipsilesional hand than those presented far from it. Here, we report the first evidence in humans that this hand-centred visual peripersonal space can be coded in relation to a seen rubber replica of the hand, as if it were a real hand. In patients with left tactile extinction, a visual stimulus presented near a seen right rubber hand induced strong cross-modal visual-tactile extinction, similar to that obtained by presenting the same visual stimulus near the patient's right hand. Critically, this specific cross-modal effect was evident when subjects saw the rubber hand as having a plausible posture relative to their own body (i.e. when it was aligned with the subject's right shoulder). In contrast, cross-modal extinction was strongly reduced when the seen rubber hand was arranged in an implausible posture (i. e. misaligned with respect to the subject's right shoulder). We suggest that this phenomenon is due to the dominance of vision over proprioception: the system coding peripersonal space can be 'deceived' by the vision of a fake hand, provided that its appearance looks plausible with respect to the subject's body. (+info)
Multimodal EEG analysis in man suggests impairment-specific changes in movement-related electric brain activity after stroke.
Movement-related slow cortical potentials and event-related desynchronization of alpha (alpha-ERD) and beta (beta-ERD) activity after self-paced voluntary triangular finger movements were studied in 13 ischaemic supratentorial stroke patients and 10 age-matched control subjects during movement preparation and actual performance. The stroke patients suffered from central arm paresis (n = 8), somatosensory deficits (n = 3) or ideomotor apraxia (n = 2). The multimodal EEG analysis suggested impairment-specific changes in the movement-related electrical activity of the brain. The readiness potential of paretic subjects was centred more anteriorly and laterally; during movement, they showed increased beta-ERD at left lateral frontal recording sites. Patients with somatosensory deficits showed reduced alpha-ERD and beta-ERD during both movement preparation and actual performance. Patients with ideomotor apraxia showed more lateralized frontal movement-related slow cortical potentials during both movement preparation and performance, and reduced left parietal beta-ERD during movement preparation. We conclude that (i) disturbed motor efference is associated with an increased need for excitatory drive of pyramidal cells in motor and premotor areas or an attempt to drive movements through projections from these areas to brainstem motor systems during movement preparation; (ii) an undisturbed somatosensory afference might contribute to the release of relevant cortical areas from their 'idling' state when movements are prepared and performed; and (iii) apraxic patients have a relative lack of activity of the mesial frontal motor system and the left parietal cortex, which is believed to be part of a network subserving ideomotor praxis. (+info)
Multisensory integration: attending to seen and felt hands.
The neglect of one side of space exhibited by some brain-damaged patients can be ameliorated by cueing the patient to the neglected side of space. A related effect has been found to depend on the hand being seen and felt at the same time. The results add to a growing literature on somatosensory-visual interactions. (+info)
Delayed onset mixed involuntary movements after thalamic stroke: clinical, radiological and pathophysiological findings.
Although occurrence of involuntary movements after thalamic stroke has occasionally been reported, studies using a sufficiently large number of patients and a control population are not available. Between 1995 and 1999, the author prospectively identified 35 patients with post-thalamic stroke delayed-onset involuntary movements, which included all or some degree of dystonia-athetosis-chorea-action tremor, occasionally associated with jerky, myoclonic components. A control group included 58 patients examined by the author during the same period who had lateral thalamic stroke but no involuntary movements. Demography, clinical features and imaging study results were compared. There were no differences in gender, age, risk factors, side of the lesion and follow-up periods. During the acute stage of stroke, the patients who had involuntary movements significantly more often had severe (< or = III/V) hemiparesis (50 versus 20%, P < 0.05) and severe sensory loss (in all modalities, P < 0.01) than the control group. At the time of assessment of involuntary movements, the patients with involuntary movements significantly more often had severe sensory deficit (in all modalities, P < 0.01) and severe limb ataxia (60 versus 5%, P < 0.01) than the control patients, but neither more severe motor dysfunction (7 versus 0%) nor more painful sensory symptoms (57 versus 57%). The patients with involuntary movements had a higher frequency of haemorrhagic (versus ischaemic) stroke (63 versus 31%, P < 0.05). Further analysis showed that dystonia-athetosis-chorea was closely associated with position sensory loss, whereas the tremor/myoclonic movements were related to cerebellar ataxia. Recovery of severe limb weakness seemed to augment the instability of the involuntary movements. Persistent failure of the proprioceptive sensory and cerebellar inputs in addition to successful, but unbalanced, recovery of the motor dysfunction seemed to result in a pathological motor integrative system and consequent involuntary movements in patients with relatively severe lateral-posterior thalamic strokes simultaneously damaging the lemniscal sensory pathway, the cerebellar-rubrothalamic tract and, relatively less severely, the pyramidal tract. (+info)