Chronic neurogenic facial pain: lack of response to intravenous phentolamine.

AIMS: Chronic neurogenic facial pain is commonly resistant to treatment and is often the source of significant patient morbidity. Adrenergic mechanisms are postulated to play a role in producing this type of pain, and adrenergic blocking agents are frequently used in clinical practice for pain control therapy. The analgesic effectiveness of an adrenergic blocking agent, intravenous phentolamine, was compared to saline and intravenous lidocaine in the present study using a single-blind protocol in patients with chronic neurogenic facial pain. METHODS: Thirty patients were studied whose common clinical features included pain for more than 6 months, unilateral trigeminal distribution, constant dysesthesia, and no evidence of pathology or known etiology. Phentolamine (30 mg), lidocaine (100 mg), and saline were each infused over periods of 5 to 10 minutes. Pain ratings were assessed every 4 minutes throughout each study period using a 10-point pain intensity scale. RESULTS: No patient reported subjective improvement of pain during or immediately following phentolamine or saline infusions alone. Sixteen of the 30 patients reported decreased pain following lidocaine infusion. In the majority of the patients, the duration of lidocaine analgesia was less than 30 minutes; however, some patients reported decreased pain for a longer time. CONCLUSION: The results do not support an adrenergic mechanism for chronic neurogenic facial pain. The response to lidocaine, a nonadrenergic, membrane-stabilizing agent, suggests that it may have clinical effectiveness in certain neurogenic facial pain patients.

Posttraumatic gustatory neuralgia: a clinical model of trigeminal neuropathic pain.

Six cases are reported in which the primary complaint was episodic, recurrent facial pain that was triggered by a taste stimulus. The pain first occurred days to weeks after head and neck surgery. Patients reported that a food stimulus placed in the mouth evoked episodic, electric shock-like pain in a preauricular location on the surgical side. The smell of food or, less reliably, emotional excitement could also trigger pain. Mandibular movement did not evoke the pain, and between lancinating attacks there was either no pain or only mild discomfort. Following an episode of pain, there was a refractory period during which the pain could not be elicited. Physical examination demonstrated a preauricular sensory loss of variable distribution. No abnormal sweating or vasomotor findings were clinically apparent. No odontogenic, muscular, salivary gland, neurologic, or psychologic pathology was found to explain the clinical symptoms. The pain was not relieved with standard doses of anticonvulsants that are commonly used to treat trigeminal neuralgia. The duration of the recurrent pain symptoms in this group was 8 to 132 months without remission. Gustatory neuralgia may be a discrete syndrome that results from abnormal interactions between salivary efferent fibers and trigeminal sensory afferent fibers in the injured auriculotemporal nerve. The unique features of the disorder make it a potentially useful clinical model for the investigation of autonomic/sensory interactions in neuropathic pain.

Anatomical properties of brainstem trigeminal neurons that respond to electrical stimulation of dural blood vessels.

Single unit recording studies in anesthetized cats have identified a population of neurons in the brainstem trigeminal complex that can be activated by stimulation of major dural blood vessels. Such dura-responsive neurons exhibit response properties that are appropriate for a role in the mediation of vascular head pain in that they typically exhibit nociceptive facial receptive fields whose periorbital distribution is similar to the region of referred pain evoked by dural stimulation in humans. In the present study, intracellular labelling with horseradish peroxidase was used to examine the anatomical characteristics of brainstem trigeminal neurons that respond to dural stimulation. A total of 17 neurons was labelled that responded to electrical stimulation of dural sites overlying the superior sagittal sinus or middle meningeal artery. Fourteen of these neurons also responded to electrical stimulation of the cornea. The neurons in this sample were located in the rostral two-thirds of the trigeminal nucleus caudalis and the caudalmost part of the nucleus interpolaris. Within caudalis, the neurons were located in the deeper part of the nucleus, primarily lamina V, and were concentrated ventrolaterally. The dendritic arborizations of the dura-responsive neurons typically exhibited a dorsolateral-to-ventromedial orientation and did not extend into the superficial laminae of caudalis. Dura-responsive neurons had axonal collaterals and boutons in the nucleus caudalis, nucleus interpolaris, the infratrigeminal region ventral to nucleus interpolaris, the nucleus of the solitary tract, and the medullary reticular formation. The axonal boutons within the trigeminal complex exhibited a ventrolateral distribution which largely overlapped the distribution of the somata. The results are consistent with previous evidence that dura-responsive brainstem trigeminal neurons may have a role in the mediation of dural vascular head pain and also indicate that such neurons may contribute to nociceptive processing within the dorsal horn.

Behavioral evidence of trigeminal neuropathic pain following chronic constriction injury to the rat's infraorbital nerve.

Video recordings of free behavior and responses to mechanical facial stimulation were analyzed to assess whether chronic constriction injury (CCI) to the rat's infraorbital nerve (IoN) results in behavioral alterations indicative of neuropathic pain. A unilateral CCI was produced by placing loose chromic gut ligatures around the IoN. After CCI to the IoN, rats exhibited changes in both non-evoked and evoked behavior. Behavioral changes developed in two phases. Early after CCI (postoperative days 1-15), rats showed increased face-grooming activity with face-wash strokes directed to the injured nerve territory, while the responsiveness to stimulation of this area was decreased. Later after CCI (postoperative days 15-130), the prevalence of asymmetric face grooming was reduced but remained significantly increased compared to control rats. The early hyporesponsiveness was abruptly replaced by an extreme hyperresponsiveness: all stimulus intensities applied to the injured nerve territory evoked the "maximal" response (brisk head withdrawal, avoidance behavior plus directed face grooming). This response was never observed in control rats. Concurrently, IoN ligation rats showed a limited increase in the responsiveness to stimulation of the contralateral IoN territory, and around postoperative days 30-40 the responsiveness to stimulation of facial areas outside the IoN territories also increased. The hyperresponsiveness to stimulation of the ligated IoN territory slightly decreased from 60 d postoperative. Throughout the study, IoN ligation rats showed decreased exploratory behavior, displayed more freezing-like behavior, had a slower body weight gain, and a higher defecation rate, compared to control rats. The behavioral alterations observed after CCI to the IoN are indicative of severe sensory disturbances within the territory of the injured nerve: mechanical allodynia develops after a period of relative hypo-/anesthesia during which behavioral signs of recurrent spontaneous, aversive (possibly painful) sensations (paresthesias/dysesthesias) are maximal.

Prediction of pain rehabilitation outcomes by motivation measures.

This study attempted to predict reduction in pain description, pain behaviour, and depression by measures of motivation and previous vocational development. Twenty-one patients randomly selected from an inpatient pain programme were given pre-admission the Goldberg Scale, a 2-h clinical interview synthesizing educational and vocational history, work values, interests, motivation to work, realistic assessment of pain disability and optimistic compared to pessimistic outlook towards the future. Repeated measures consisted of the McGill-Melzack Pain Questionnaire, the Pain Disability Index, and the Beck Depression Inventory, given at admission, discharge and follow-up. Pain was classified by the IASP categories. The Goldberg Scale predicted at p less than 0.05 level for reduction of subjective pain description on MMPQ and reduction of depressive symptoms on Beck, but failed to predict for reduction of pain behaviour at 0.05 level. A measure of motivation may be a useful adjunct to the broad array of measures to predict outcome in pain management programmes.

Deafferentation pain syndromes.

Neuropathic pain is a major clinical problem and is often a source of persistent suffering and disability for patients with deafferenting injuries. In addition to the emotional burden of this persistent pain, patients' lives are frequently disrupted socially and financially. Understanding of the mechanisms that underlie neuropathic pain is poor, although there is evidence for widespread changes within the peripheral and central somatosensory nervous systems of such patients. In addition, treatment for neuropathic pain is often ineffective. Some degree of symptom control is often possible, however, through a multidisciplinary approach. This approach includes medications, physical treatments, and behavioral modifications. The limited understanding we have of the mechanisms of neuropathic pain is a strong reason to actively pursue further research into the pathophysiology of these conditions. Continued clinical and basic investigations into neuropathic pain also provide the best chance of finding treatments that are effective.

Vestibular and medullary brain stem afferents to the abducens nucleus in the cat.

Brain stem neurons that project to the abducens nucleus (nVI) were labeled by the technique of retrograde transport of horseradish peroxidase (HRP). Following iontophoresis of HRP into nVI a large number of labeled cells are found in the ipsilateral vestibular nuclear complex, extending from the rostral medial vestibular nucleus into the ventral lateral vestibular nucleus. A smaller number of HRP-positive cells are also found in the contralateral medial vestibular nucleus. In addition, labeled cells are localized to the contralateral dorsomedial gigantocellular tegmental field as well as the nucleus praepositus hypoglossi of both sides, evidence that these neuronal groups may also be involved in eye movement control.