Concurrent Bell's Palsy and Facial Pain Improving with Multimodal Chiropractic Therapy: A Case Report and Literature Review.

BACKGROUND Bell's palsy, also called facial nerve palsy, occasionally co-occurs with trigeminal neuropathy, which presents as additional facial sensory symptoms and/or neck pain. Bell's palsy has a proposed viral etiology, in particular when occurring after dental manipulation. CASE REPORT A 52-year-old Asian woman presented to a chiropractor with a 3-year history of constant neck pain and left-sided maxillary, eyebrow, and temporomandibular facial pain, paresis, and paresthesia, which began after using a toothpick, causing possible gum trauma. She had previously been treated with antiviral medication and prednisone, Chinese herbal medicine, and acupuncture, but her recovery plateaued at 60% after 1 year. The chiropractor ordered cervical spine magnetic resonance imaging, which demonstrated cervical spondylosis, with no evidence of myelopathy or major pathology. Treatment involved cervical and thoracic spinal manipulation, cervical traction, soft-tissue therapy, and neck exercises. The patient responded positively. At 1-month follow-up, face and neck pain and facial paresis were resolved aside from residual eyelid synkinesis. A literature review identified 12 additional cases in which chiropractic spinal manipulation with multimodal therapies was reported to improve Bell's palsy. Including the current case, 85% of these patients also had pain in the face or neck. CONCLUSIONS This case illustrates improvement of Bell's palsy and concurrent trigeminal neuropathy with multimodal chiropractic care including spinal manipulation. Limited evidence from other similar cases suggests a role of the trigeminal pathway in these positive treatment responses of Bell's palsy with concurrent face/neck pain. These findings should be explored with research designs accounting for the natural history of Bell's palsy.

Long lasting trigeminal neuropathy, limbic encephalitis and abdominal ganglionitis without primary cancer: An atypical case of Hu-antibody syndrome.

OBJECTIVES: Anti-Hu antibodies (Hu-Abs) are the most frequent onconeural antibodies associated with paraneoplastic neurologic syndromes (PNS). PNS include a variety of neurological syndromes, affecting less than 1/10,000 patients with cancer. In the majority of cases, PNS will manifest before the malignancy is diagnosed. We found a case in which PNS was diagnosed without finding a primary malignancy after extensive work-up and even post-mortem autopsy. PATIENT AND METHODS: We present a case report of a 58-year-old man. This article includes extensive clinical work-up, full-body autopsy and brain autopsy with classical histochemical and myelin stainings and immunohistochemistry was performed. RESULTS: The patient developed a progressive trigeminal neuropathy over a period of 5 years, in combination with cerebellar degeneration, asymmetrical brainstem and limbic encephalitis. Serum showed repeatedly high anti-Hu antibodies. Comprehensive cancer screening could not demonstrate any primary malignancy. Therapy with corticosteroids, plasma exchange, cyclophosphamide and rituximab showed no beneficial effect. He died from the complications of enteric ganglionitis 5 years after onset of the first symptoms. A postmortem autopsy could not detect a primary malignancy either. Brain morphology is described in detail. CONCLUSION: Paraneoplastic anti-Hu encephalitis cases associated with SCLC or other primary neoplasms are well known. An adult with a progressive multifocal neurological syndrome in the presence of positive anti-Hu antibodies, but without any primary neoplasm after a follow-up over 5 years is unusual.

Neuromodulation of the lingual nerve: a novel technique.

Acute injury of the trigeminal nerve or its branches can result in posttraumatic trigeminal neuropathy (PTTN). Affected patients suffer from chronic debilitating symptoms long after they have recovered from the inciting trauma. Symptoms vary but usually consist of paresthesia, allodynia, dysesthesia, hyperalgesia, or a combination of these symptoms. PTTN of the trigeminal nerve can result from a variety of traumas, including iatrogenic injury from various dental and maxillofacial procedures. Treatments include medications, pulsed radiofrequency modulation, and microsurgical repair. Although trigeminal nerve stimulation has been reported for trigeminal neuropathy, V3 implantation is often avoided because of an elevated migration risk secondary to mandibular motion, and lingual nerve implantation has not been documented. Here, the authors report on a patient who suffered from refractory PTTN despite multiple alternative treatments. He elected to undergo novel placement of a lingual nerve stimulator for neuromodulation therapy. To the best of the authors' knowledge, this is the first documented case of lingual nerve stimulator implantation for lingual neuropathy, a technique for potentially reducing the risk of electrode migration.

Dopamine receptor D2, but not D1, mediates descending dopaminergic pathway-produced analgesic effect in a trigeminal neuropathic pain mouse model.

Neuropathic pain represents a challenge to clinicians because it is resistant to commonly prescribed analgesics due to its largely unknown mechanisms. Here, we investigated a descending dopaminergic pathway-mediated modulation of trigeminal neuropathic pain. We performed chronic constriction injury of the infraorbital nerve from the maxillary branch of trigeminal nerve to induce trigeminal neuropathic pain in mice. Our retrograde tracing showed that the descending dopaminergic projection from hypothalamic A11 nucleus to spinal trigeminal nucleus caudalis is bilateral. Optogenetic/chemogenetic manipulation of dopamine receptors D1 and D2 in the spinal trigeminal nucleus caudalis produced opposite effects on the nerve injury-induced trigeminal neuropathic pain. Specific excitation of dopaminergic neurons in the A11 nucleus attenuated the trigeminal neuropathic pain through the activation of D2 receptors in the spinal trigeminal nucleus caudalis. Conversely, specific ablation of the A11 dopaminergic neurons exacerbated such pain. Our results suggest that the descending A11-spinal trigeminal nucleus caudalis dopaminergic projection is critical for the modulation of trigeminal neuropathic pain and could be manipulated to treat such pain.

Impaired Corneal Sensation and Nerve Loss in a Type 2 Rat Model of Chronic Diabetes Is Reversible With Combination Therapy of Menhaden Oil, α-Lipoic Acid, and Enalapril.

PURPOSE: This study investigated the efficacy of monotherapy versus combination of menhaden oil, α-lipoic acid, and enalapril on corneal sensation and morphometry and other neuropathy-related endpoints in a rat model of type 2 diabetes. METHODS: Male Sprague-Dawley rats (aged 12 weeks) were fed a high-fat diet for 8 weeks followed by 30 mg/kg streptozotocin. After 16 weeks of hyperglycemia, 12-week treatments consisting of menhaden oil, α-lipoic acid, enalapril, or their combination were initiated. Before and after treatments, we performed analyses of multiple neural and vascular endpoints including corneal sensitivity, corneal nerve density, vascular reactivity of epineurial arterioles, motor and sensory nerve conduction velocity, intraepidermal nerve fiber density, and thermal nociception. RESULTS: Before treatment, all the neural and vascular endpoints in diabetic rats were impaired. Treating diabetic rats with monotherapy was effective in improving neural and vascular deficits with menhaden oil being most efficacious. However, the combination therapy provided the greatest benefit and improved/reversed all nerve and vascular deficits. The effect of combination therapy on corneal relative sensitivity and structure (in mm/mm), primary endpoints for this study, for control, diabetic, and diabetic treated rats was 4.2 ± 1.4 and 7.5 ± 0.5, 12.1 ± 1.3* and 3.8 ± 0.2*, and 6.6 ± 2.3 and 7.3 ± 0.5, respectively (*P < 0.05 compared with control rats; P < 0.05 compared with diabetic rats). CONCLUSIONS: These studies suggest that a combination therapeutic approach may be most effective for treating vascular and neural complications of type 2 diabetes.

Stimulation of the Gasserian ganglion in the treatment of refractory trigeminal neuropathy.

OBJECTIVES: We evaluated the effectiveness of a custom-made neurostimulator with which to treat patients for refractory trigeminal neuropathic pain (TNP) at the level of the Gasserian ganglion. MATERIALS AND METHODS: A retrospective analysis of 22 patients referred to our pain clinic, AZ Sint-Nikolaas, between 2010 and 2015, was conducted using the McGill Pain and EuroQoL questionnaire before, two weeks after, and at the final follow-up after neurostimulator treatment. RESULTS: Successful test stimulations were achieved for 77.3% of patients, with satisfactory long-term pain relief reported by 44% at 24 months. The predictive value of the trial stimulation was 80%, with 82.4% of patients reporting one or more complication, the most common being neck discomfort due to fibrosis. A small cohort size (22) limited our statistical analyses. However younger patients presented with a higher incidence of negative results after 24 months or physical complications. Cut-off ages were set at the age of 62 and 58 years respectively. CONCLUSION: Stimulation of the Gasserian ganglion is a promising technique for the treatment of refractory TNP and should be considered ahead of more invasive techniques such as motor cortex or deep brain stimulation. The referral of refractory TNP patients should also be accomplished as early as possible to improve outcome.

An update on the causes, assessment and management of third division sensory trigeminal neuropathies.

Introduction Sensory neuropathies of the mandibular division of the trigeminal (V3) nerve can be debilitating, causing difficulty with daily function. It has a variety of causes, including iatrogenic injury, usually caused by third molar removal, local anaesthetic administration, implant placement or endodontic treatment. Non-iatrogenic causes include infection, primary or secondary neoplasia and various medical conditions.Objective To review the aetiology, evaluation and management of V3 neuropathy in a retrospective case-series of patients referred to a specialist nerve injury clinic over an eight-year period, particularly focusing on the non-iatrogenic causes of this presentation.Methods A retrospective analysis of the case notes of 372 patients referred to the specialist nerve injury clinic between 2006 and 2014 was carried out to establish the cause of the neuropathy and subsequent management or referral. The assessment protocol of trigeminal neuropathy used in the clinic is also outlined.Results Most patients (89.5%) presented with neuropathy due to iatrogenic injury. Of the non-iatrogenic causes (10.5%), malignancy accounted for a fifth of presentations, and infection almost two-fifths, demonstrating the importance of prompt identification of a cause and management by the clinician, or referral to the appropriate specialty. Other, more rare causes are also presented, including multiple sclerosis, sickle-cell anaemia and Paget's disease, highlighting the importance to the clinician of considering differential diagnoses.Conclusions This case series demonstrates the less frequent, but nevertheless important, non-iatrogenic causes which clinicians should consider when assessing patients with trigeminal neuropathy.

Peripheral nerve field stimulation for trigeminal neuralgia, trigeminal neuropathic pain, and persistent idiopathic facial pain.

OBJECTIVE: Peripheral nerve field stimulation (PNFS) is a promising modality for treatment of intractable facial pain. However, evidence is sparse. We are therefore presenting our experience with this technique in a small patient cohort. METHODS: Records of 10 patients (five men, five women) with intractable facial pain who underwent implantation of one or several subcutaneous electrodes for trigeminal nerve field stimulation were retrospectively analyzed. Patients' data, including pain location, etiology, duration, previous treatments, long-term effects and complications, were evaluated. RESULTS: Four patients suffered from recurrent classical trigeminal neuralgia, one had classical trigeminal neuralgia and was medically unfit for microvascular decompression. Two patients suffered from trigeminal neuropathy attributed to multiple sclerosis, one from post-herpetic neuropathy, one from trigeminal neuropathy following radiation therapy and one from persistent idiopathic facial pain. Average patient age was 74.2 years (range 57-87), and average symptom duration was 10.6 years (range 2-17). Eight patients proceeded to implantation after successful trial. Average follow-up after implantation was 11.3 months (range 5-28). Using the visual analog scale, average pain intensity was 9.3 (range 7-10) preoperatively and 0.75 (range 0-3) postoperatively. Six patients reported absence of pain with stimulation; two had only slight constant pain without attacks. CONCLUSION: PNFS may be an effective treatment for refractory facial pain and yields high patient satisfaction.

Trigeminal Ganglion Stimulation.

Facial pain in the distribution of the trigeminal nerve, commonly identified as trigeminal neuralgia, should not be confused with trigeminal neuropathic pain. The latter is caused by an accidental and nonintentional nerve lesion. When the first-line pharmacological treatment fails to provide satisfactory pain relief, surgical treatment, such as microvascular decompression and neurodestructive interventions (radiofrequency or cryotherapy), is not indicated. The logical choice of technique becomes neuromodulation, but it may be challenging to perform in the facial area. Although the initial results of trigeminal ganglion stimulation were promising, they often were of short duration because of lead migration and inadequate stimulation coverage in the trigeminal nerve distribution. To ensure accurate placement and proper anchoring, a custom-made electrode was developed and produced, and its stereotactic implantation is guided by electromagnetic navigation. This technique has been used at our center for several years; the published results show at least 30% of pain relief in 75% of the patients and considerable reduction in medication use.

[Analgesic effect of CQM on prosopalgia model rats and its impact on exciting amino acid neurotransmitters].

OBJECTIVE: To observe the analgesic effect of CQM on photochemically-induced prosopalgia model rats, and discuss its impact on the exciting amino acid neurotransmitter-glutamate (Glu). METHOD: Male SD rats were randomly divided into the sham operation group and the prosopalgia group. And the latter was subdivided into the model group, the gabapentin group (100 mg kg(-1)), and the CQM low-dose (35 mg x kg(-1)) and CQM high-dose (70 mg x kg(-1)) groups. The mechanical allodynia test was adopted to evaluate the pain behavior of rats, and reflect the efficacy with the mechanical withdrawal thresholds. The rat striatum extra-cellular fluid was collected by brain micro-dialysis. The Glu level of samples was measured by high performance liquid chromatography-fluorescene detector (HPLC-FLD). RESULT: Compared to the control group, the threshold of the mechanical allodynia of the IoN injury group was decreased significantly (P < 0.05), and the concentration of Glu was increased dramatically (P < 0.05). Compared to the model group, the mechanical allodynia of photochemically-induced prosopalgia model rats increased significantly (P < 0.01), with a notable increase in brain Glu concentration (P < 0.05). Compared with the model group, all of mechanical withdrawal thresholds increased. Among them, the CQM high-dose group showed a remarkably growth at three time points (P < 0.05), with the maximum up to (23 +/- 7.3) g. And the gabapentin group showed a remarkably growth at two time points (P < 0.05), with the maximum up to (20.5 +/- 9.2) g. All of the drug groups showed significantly lower Glu concentrations in rat brains than the model group (P < 0.05). CONCLUSION: CQM can ease the mechanical allodynia of photochemically-induced prosopalgia model rats. Its analgesic effect may be related to the decrease of Glu concentrations in striatum extra-cellular fluid.

Analgesic effect of CQM on prosopalgia model rats and its impact on exciting amino acid neurotransmitters / 中国中药杂志

<p><b>OBJECTIVE</b>To observe the analgesic effect of CQM on photochemically-induced prosopalgia model rats, and discuss its impact on the exciting amino acid neurotransmitter-glutamate (Glu).</p><p><b>METHOD</b>Male SD rats were randomly divided into the sham operation group and the prosopalgia group. And the latter was subdivided into the model group, the gabapentin group (100 mg kg(-1)), and the CQM low-dose (35 mg x kg(-1)) and CQM high-dose (70 mg x kg(-1)) groups. The mechanical allodynia test was adopted to evaluate the pain behavior of rats, and reflect the efficacy with the mechanical withdrawal thresholds. The rat striatum extra-cellular fluid was collected by brain micro-dialysis. The Glu level of samples was measured by high performance liquid chromatography-fluorescene detector (HPLC-FLD).</p><p><b>RESULT</b>Compared to the control group, the threshold of the mechanical allodynia of the IoN injury group was decreased significantly (P < 0.05), and the concentration of Glu was increased dramatically (P < 0.05). Compared to the model group, the mechanical allodynia of photochemically-induced prosopalgia model rats increased significantly (P < 0.01), with a notable increase in brain Glu concentration (P < 0.05). Compared with the model group, all of mechanical withdrawal thresholds increased. Among them, the CQM high-dose group showed a remarkably growth at three time points (P < 0.05), with the maximum up to (23 +/- 7.3) g. And the gabapentin group showed a remarkably growth at two time points (P < 0.05), with the maximum up to (20.5 +/- 9.2) g. All of the drug groups showed significantly lower Glu concentrations in rat brains than the model group (P < 0.05).</p><p><b>CONCLUSION</b>CQM can ease the mechanical allodynia of photochemically-induced prosopalgia model rats. Its analgesic effect may be related to the decrease of Glu concentrations in striatum extra-cellular fluid.</p>

Ramsay Hunt syndrome with unilateral polyneuropathy involving cranial nerves V, VII, VIII, and XII in a diabetic patient.

Ramsay Hunt syndrome is a rare complication of the varicella zoster virus, defined as a peripheral facial palsy that typically results from involvement of the facial and auditory nerves. Ramsay Hunt syndrome can be associated with cranial nerves V, VI, IX, and X but rarely with XII. We describe an atypical case of Ramsay Hunt syndrome with multiple cranial nerve involvement of nerves V, VII, VIII, and XII. Antiviral drugs, antibiotics, insulin, and traditional Chinese drugs were administered immediately after admission. After 3 months of combination therapy, the patient had recovered satisfactorily. Herpes zoster can cause severe infections in diabetic patients and should be treated as soon after detection as possible. Ramsay Hunt syndrome should be recognized as a polycranial neuritis characterized by damage to sensory and motor nerves. In addition to facial and vestibular nerve paralysis, Ramsay Hunt syndrome may also involve cranial nerves V and XII.

Sensory retraining: a cognitive behavioral therapy for altered sensation.

Sensory retraining teaches the patient to ignore or blot out postinjury unpleasant orofacial sensations to optimally tune into and decipher the weakened and damaged signals from the tissues. Sensory retraining is a simple, inexpensive, noninvasive exercise program, which initiated shortly after injury, can lessen the objectionable impression of orofacial altered sensations. Sensory retraining exercises are most effective on decreasing the perceived burden associated with hypoesthetic orofacial altered sensations.

Motor cortex stimulation for trigeminal neuropathic or deafferentation pain: an institutional case series experience.

BACKGROUND: Trigeminal neuropathy is a rare, devastating condition that can be intractable and resistant to treatment. When medical treatment fails, invasive options are limited. Motor cortex stimulation (MCS) is a relatively recent technique introduced to treat central neuropathic pain. The use of MCS to treat trigeminal neuropathic or deafferentation pain is not widespread and clinical data in the medical literature that demonstrate efficacy are limited. METHOD: We retrospectively reviewed patients with trigeminal neuropathic or trigeminal deafferentation pain who were treated at the Oregon Health & Science University between 2001 and 2008 by 1 neurosurgeon using MCS. RESULTS: Eight of 11 patients (3 male, 8 female) underwent successful permanent implantation of an MCS system. All 8 patients reported initial satisfactory pain control. Three failed to experience continued pain control (6 months of follow-up). Five continued to experience long-term pain control (mean follow-up, 33 months). Average programming sessions were 2.2/year (all 8 patients) and 1.55/year (5 patients who sustained long-term pain control). Patients with anesthesia dolorosa or trigeminal deafferentation pain who had previously undergone ablative trigeminal procedures responded poorly to MCS. We encountered no perioperative complications. CONCLUSION: MCS is a safe and potentially effective therapy in certain patients with trigeminal neuropathy.

[Analgesic effect of Corydalis yanhusuo in a rat model of trigeminal neuropathic pain].

OBJECTIVE: To evaluate the analgesic effect of Corydalis yanhusuo on trigeminal neuropathic pain.in a rat model. METHOD: Rat model of trigeminal neuralgia pain were established by inducing chronic constriction injury (CCI) of the infraorbital branch of the trigeminal nerve (ION). The effect of Corydalis yanhusuo, a traditional Chinese medicine, in ameliorating the pain was tested. Western blotting was performed to investigate the change of cannabinoid CB1 receptors in the Vc the injury of the infraorbital branch of the trigeminal nerve (ION-CCI). CB1 receptor antagonist AM 251 was applied to observe its effect on the analgesic effect of Yanhusuo. RESULT: Administration of dl-THP (2 mg/kg) intraperitoneally increased the response threshold and the cut-off threshold to the mechanical stimulation in ION-CCI rat models. ION-CCI induced an upregulation of cannabinoid CB1 receptors within the ipsilateral of Vc. The effect of Yanhusuo was antagonized by the application of AM 251. CONCLUSION: The analgesic effect of Yanhusuo involves the participation of CB1 receptors, suggesting that Yanhusuo may offer a useful therapeutic approach for trigeminal neuropathic pain.

Can chronic irritations of the trigeminal nerve cause musculoskeletal disorders?

In this article, five cases of odontogenous dysfunctions and musculoskeletal complaints are presented. A common finding in all patients of this study was that the presence of joint complaints was related to deficits in the corresponding muscular function. These deficits were determined by manual muscle tests as described by Kendall et al. [Muscles - Testing and Function, ed 4. Baltimore, Williams and Wilkins, 1993] and were eliminated immediately by a neural therapeutic test injection into the disturbed dental region. The therapy provided solely aimed to eliminate the odontogenous dysfunction. No other therapeutic measures were carried out with regard to the patients' respective muscle, tendon, or joint complaints.

Analgesic effect of Corydalis yanhusuo in a rat model of trigeminal neuropathic pain / 南方医科大学学报

<p><b>OBJECTIVE</b>To evaluate the analgesic effect of Corydalis yanhusuo on trigeminal neuropathic pain.in a rat model.</p><p><b>METHOD</b>Rat model of trigeminal neuralgia pain were established by inducing chronic constriction injury (CCI) of the infraorbital branch of the trigeminal nerve (ION). The effect of Corydalis yanhusuo, a traditional Chinese medicine, in ameliorating the pain was tested. Western blotting was performed to investigate the change of cannabinoid CB1 receptors in the Vc the injury of the infraorbital branch of the trigeminal nerve (ION-CCI). CB1 receptor antagonist AM 251 was applied to observe its effect on the analgesic effect of Yanhusuo.</p><p><b>RESULT</b>Administration of dl-THP (2 mg/kg) intraperitoneally increased the response threshold and the cut-off threshold to the mechanical stimulation in ION-CCI rat models. ION-CCI induced an upregulation of cannabinoid CB1 receptors within the ipsilateral of Vc. The effect of Yanhusuo was antagonized by the application of AM 251.</p><p><b>CONCLUSION</b>The analgesic effect of Yanhusuo involves the participation of CB1 receptors, suggesting that Yanhusuo may offer a useful therapeutic approach for trigeminal neuropathic pain.</p>

A successful combined endovascular and surgical treatment of a cranial base mucormycosis with an associated internal carotid artery pseudoaneurysm.

OBJECTIVE: We report a rare case of internal carotid artery pseudoaneurysm owing to rhinocerebral mucormycosis and review 40 reported cases from 1980 to present. CLINICAL PRESENTATION: A 38-year-old Caucasian man presented with a 3-day history of headache, diplopia, and numbness in the distribution of the left ophthalmic and maxillary branches of the trigeminal nerve. A complete left cavernous syndrome was discovered upon neurological examination. Magnetic resonance imaging scans revealed an inflammatory process involving the paranasal sinuses with extension into the left cavernous sinus, temporal fossa, and petrous bone. INTERVENTION: The patient was immediately treated with amphotericin B, atorvastatin, and daily hyperbaric oxygen sessions before surgical intervention. The patient underwent endovascular treatment of the associated mycotic pseudoaneurysm after carotid test occlusion in addition to a radical bilateral debridement of the paranasal sinuses and infratemporal and temporal fossa. CONCLUSION: Aggressive multimodal therapy is imperative for late-stage rhinocerebral mucormycosis. Extensive resection of infected tissue combined with amphotericin B, atorvastatin, and hyperbaric oxygen seems to be the best course of management. If the internal carotid artery is involved, endovascular intervention is clearly an option to attain this goal. Further research and longer follow-up periods are required to better understand the long-term implications of endovascular coiling and hyperbaric oxygen therapy for rhinocerebral mucormycosis.

Effects of removal of dietary polyunsaturated fatty acids on plasma extravasation and mechanical allodynia in a trigeminal neuropathic pain model.

BACKGROUND: Neuropathic pain (NP) is partially mediated by neuroinflammatory mechanisms, and also modulates local neurogenic inflammation. Dietary lipids, in particular the total amount and relative proportions of polyunsaturated fatty acids (PUFAs) of the omega-3 and omega-6 families, have been reported to modify the threshold for thermal and mechanical allodynia in the partial sciatic nerve ligation model of NP in rats. The effects of dietary lipids on other popular NP models, such as the chronic constriction injury (CCI), have not yet been examined. It is also unknown whether dietary PUFAs exert any effect on the capsaicin (CAP)-induced neurogenic inflammation under control or NP conditions. In this study we investigated these interrelated phenomena in the trigeminal territory, which has been much less explored, and for which not all data derived from limb nerves can be directly applied. RESULTS: We studied the effects of a CCI of the infraorbital nerve (IoN) on the development of mechanical allodynia and CAP-induced plasma extravasation in rats fed either a regular diet (RD), or a modified diet (MD) with much lower total content and omega-3:omega-6 ratio of PUFAs. In rats kept on MD, mechanical allodynia following CCI-IoN was more pronounced and developed earlier. Extravasation was substantially increased in naive rats fed MD, and displayed differential diet-depending changes one and four weeks after CCI-IoN. When compared with basal levels (in naive and/or sham cases), the net effect of CCI-IoN on ipsilateral extravasation was a reduction in the MD group, but an increase in the RD group, effectively neutralizing the original intergroup differences. CONCLUSION: In summary, PUFA intake reduces CAP-induced neurogenic plasma extravasation in the trigeminal territory, and their removal significantly alters the mechanical allodynia and the plasma extravasation that result from a unilateral CCI-IoN. It is likely that this "protective" effect of dietary lipids is temporary. Also, the presence of contralateral effects of CCI-IoN precludes using the contralateral side as control.

Lyme disease with lymphocytic meningitis, trigeminal palsy and silent thalamic lesion.

We describe a follow-up in a 15-year-old boy with neuroborreliosis diagnosed by clinical symptoms, CSF and serum analysis. MRI revealed a thalamic lesion and an enhancement of the right trigeminal nerve clinically associated with mild hypasthesia in the right maxillary region. Both, clinical symptoms and radiological findings disappeared within 2 months after treatment. Borrelia burgdorferi specific IgM and IgG in CSF and IgG in serum became negative between 6 and 12 months after diagnosis. We show that neuroborreliosis at an early stage may present only with moderate neurological deficits and that at this stage MRI reveals distinct cerebral lesions which might even precede clinical manifestation. Thus, early diagnosis and treatment of neuroborreliosis may prevent persistent neurologic lesions.