Bladder outlet obstruction causes up-regulation of nicotinic acetylcholine receptors in bladder-projecting pelvic ganglion neurons.

Pelvic ganglion (PG) neurons relay sympathetic and parasympathetic signals to the lower urinary tract, comprising the urinary bladder and bladder outlet, and are thus essential for both storage and voiding reflexes. Autonomic transmission is mediated by activation of the nicotinic acetylcholine receptor (nAChR) in PG neurons. Previously, bladder outlet obstruction (BOO), secondary to benign prostatic hyperplasia, was found to increase soma sizes of bladder-projecting PG neurons. To date, however, it remains unknown whether these morphological changes are accompanied by functional plasticity in PG neurons. In the present study, we investigated whether BOO alters acetylcholine receptor (nAChR) transcript expression and current density in bladder PG neurons. Partial ligation of the rat urethra for six weeks induced detrusor overactivity (DO), as observed during cystometrical measurement. In rats exhibiting DO, membrane capacitance of parasympathetic bladder PG neurons was selectively increased. Real-time PCR analysis revealed that BOO enhanced the expression of the transcripts encoding the nAChR α3 and ß4 subunits in PG neurons. Notably, BOO significantly increased ACh-evoked current density in parasympathetic bladder PG neurons, whereas no changes were observed in sympathetic bladder and parasympathetic penile PG neurons. In addition, other ligand-gated ionic currents were immune to BOO in bladder PG neurons. Taken together, these data suggest that BOO causes upregulation of nAChR in parasympathetic bladder PG neurons, which in turn may potentiate ganglionic transmission and contribute to the development of DO.

The nervus intermedius: a review of its anatomy, function, pathology, and role in neurosurgery.

BACKGROUND: Geniculate neuralgia, although uncommon, can be a debilitating pathology. Unfortunately, a thorough review of this pain syndrome and the clinical anatomy, function, and pathology of its most commonly associated nerve, the nervus intermedius, is lacking in the literature. Therefore, the present study aimed to further elucidate the diagnosis of this pain syndrome and its surgical treatment based on a review of the literature. METHODS: Using standard search engines, the literature was evaluated for germane reports regarding the nervus intermedius and associated pathology. A summary of this body of literature is presented. RESULTS: Since 1968, only approximately 50 peer-reviewed reports have been published regarding the nervus intermedius. Most of these are single-case reports and in reference to geniculate neuralgia. No report was a review of the literature. CONCLUSIONS: Neuralgia involving the nervus intermedius is uncommon, but when present, can be life altering. Microvascular decompression may be effective as a treatment. Along its cisternal course, the nerve may be difficult to distinguish from the facial nerve. Based on case reports and small series, long-term pain control can be seen after nerve sectioning or microvascular decompression, but no prospective studies exist. Such studies are now necessary to shed light on the efficacy of surgical treatment of nervus intermedius neuralgia.

Painful sweating.

OBJECTIVE: The authors report a case of spontaneous and gustatory facial pain and sweating. METHODS: The patient had frequent episodes of pain, sweating, and flushing bilaterally in the hairless skin of the ophthalmic and maxillary distributions of the trigeminal nerve. Gustatory stimuli (e.g., orange juice, pickled onions) reliably evoked episodes, but episodes also frequently came on spontaneously. The problem had begun during adolescence, about the time of topical treatment and then electrocauteries for facial warts. The patient reported benefit from tricyclic antidepressants, guanethidine, and trospium chloride (an anti-cholinergic quaternary amine used in Europe for urinary urgency). There was no pain or excessive sweating in other body areas, nor pain with exercise. RESULTS: Administration of edrophonium IV evoked pain and sweating, and ganglion blockade by IV trimethaphan eliminated pain and sweating and markedly attenuated responses to edrophonium. Trospium chloride also prevented edrophonium-induced pain and sweating. Bicycle exercise produced the same increment in forehead humidity as in a spontaneous episode but did not evoke pain. Tyramine infusion did not bring on pain or sweating, whereas iontophoretic acetylcholine administration to one cheek evoked pain and sweating bilaterally. Topical glycopyrrolate cream eliminated spontaneous, gustatory, and edrophonium-induced episodes. CONCLUSIONS: The findings indicate that facial pain and sweating can result from occupation of muscarinic cholinergic receptors after acetylcholine release from local nerves. The authors propose that after destruction of cutaneous nerves, aberrant regenerant sprouting innervates sweat glands, producing gustatory sweating as in auriculotemporal syndrome (Frey syndrome), and innervates nociceptors, producing pain.

Pupillography refines the diagnosis of diabetic autonomic neuropathy.

Although diabetic autonomic neuropathy involves most organs, diagnosis is largely based on cardiovascular tests. Light reflex pupillography (LRP) non-invasively evaluates pupillary autonomic function. We tested whether LRP demonstrates autonomic pupillary dysfunction in diabetics independently from cardiac autonomic neuropathy (CAN) or peripheral neuropathy (PN). In 36 type-II diabetics (39-84 years) and 36 controls (35-78 years), we performed LRP. We determined diameter (PD), early and late re-dilation velocities (DV) as sympathetic parameters and reflex amplitude (RA) and constriction velocity (CV) as parasympathetic pupillary indices. We assessed the frequency of CAN using heart rate variability tests and evaluated the frequency of PN using neurological examination, nerve conduction studies, thermal and vibratory threshold determination. Twenty-eight (77.8%) patients had abnormal pupillography results, but only 20 patients (56%) had signs of PN or CAN. In nine patients with PN, only pupillography identified autonomic neuropathy. Four patients had pupillary dysfunction but no CAN or PN. In comparison to controls, patients had reduced PD, late DV, RA and CV indicating sympathetic and parasympathetic dysfunction. The incidence and severity of pupillary abnormalities did not differ between patients with and without CAN or PN. LRP demonstrates sympathetic and parasympathetic pupillary dysfunction independently from PN or CAN and thus refines the diagnosis of autonomic neuropathy in type-II diabetics.

Quantitative assessment and correlation of sympathetic, parasympathetic, and afferent small fiber function in peripheral neuropathy.

We compared three neurophysiological methods for assessing small nerve fiber function in 40 patients with peripheral neuropathy to determine the various manifestation types of peripheral small fiber neuropathy. Heart rate variation tests were used to assess cardiac parasympathetic small fiber function. Cutaneous vasoconstrictor responses (sympathetic C fibers) induced by deep inspiration were examined with laser Doppler flowmetry. Cutaneous afferent C fiber function was assessed by measurement of axon reflex vasodilatation induced by histamine iontophoresis. All test parameters were significantly lower in patients with peripheral neuropathy than in control subjects. Comparison of the three small fiber systems revealed that functionally different systems are damaged independently, and isolated affection of each fiber type was frequently observed. The three tests are useful noninvasive tools with which to evaluate sympathetic, parasympathetic, and afferent small fiber function in patients with peripheral neuropathy. In many patients functionally different small fiber systems are affected selectively. To diagnose small fiber neuropathy and to evaluate the individual type of manifestation complementary testing of several small somatic and autonomic fiber systems is necessary.