[Toxic leucoencephalopathy after use of sniffed heroin, an unrecognized form of beneficial evolution]. / Leucoencéphalopathie toxique après consommation d'héroïne prisée "sniff", une forme méconnue d'évolution favorable.

INTRODUCTION: Serious leukoencephalopathy can be related to heroin injection or inhalation. OBSERVATION: We report the first case of leukoencephalopathy observed three weeks after a 46-year-old man sniffed heroin. The clinical presentation included cognitive and behaviour disorders, pyramidal irritation and slight gait instability. Blood and cerebrospinal fluid analyse were normal. Brain magnetic resonance imaging showed diffuse, symmetrical supratentorial white matter lesions producing high intense signals on FLAIR and b1000-weighted sequences. Proton spectroscopy revealed an increased rate of cholin, in favour of active demyelinated lesions. Brain biopsy showed intramyelinic oedema with reactive gliosis. After two and a half years, moderate attentional fluctuations and difficulties in initiating activities persisted. Repeated MRI showed a reduction of the leukoencephalopathy. CONCLUSION: Heroin could be a cause more common than thought of leukoencephalopathy. The clinical and radiological expression and prognosis could be related to the mode of consummation (inhalation, intravenous injection, sniffing). This parameter may modulate severity and localization of brain lesions. More systematic use of MRI for patients with psychiatric symptoms after heroin intoxications could lead to a better evaluation of heroin-related neurotoxicity and potentially improve prevention.

[Brain abscess as the first clinical manifestation of isolated pulmonary arteriovenous malformation without Rendu-Osler disease]. / Abcès cérébelleux révélant une malformation artérioveineuse pulmonaire isolée en dehors de la maladie de Rendu-Osler.

INTRODUCTION: Brain abscesses occur in 5 to 13 % of patients with pulmonary arteriovenous malformation (PAVM), more often present in Rendu-Osler-Weber disease or hereditary hemorrhagic telangiectasia (HHT). CASE REPORT: A 51-year-old man with a history of transient Parinaud syndrome at 37 years complained of headache for 2 months before acute onset of a left cerebellar syndrome without fever. CT-scan and MRI of the head revealed a heterogeneous left cerebellar lesion. A brain abscess was drained and all signs resolved. CT-scan of the chest revealed a left lingual PAVM; occlusion was incomplete after coil embolization. He had no feature of HHT and no mutation in ENG and ACVRL1 genes. A second embolization was performed 5 months later, but the malformation was not occluded at 6 months. DISCUSSION: We report the seventh case of PAVM complicated by a cerebellar abscess. The right to left shunt in PAVM results in hypoxemia, secondary polycythemia and paradoxical embolization of infective organisms bypassing the pulmonary filter. CONCLUSION: Combining different MRI techniques (in particular diffusion and proton MR spectroscopy) provides invaluable data for the diagnosis of brain abscess. Careful search for PAVM must be undertaken, particularly in adults with cryptogenic abscess, to avoid further abscess formation or stroke.

[Post-traumatic focal fixed dystonia of the shoulder: a distinctive syndrome with speculative mechanisms?]. / Dystonie focale fixée de l'épaule à distance d'un traumatisme scapulaire minime : une entité pour quels mécanismes ?

INTRODUCTION: Whether post-traumatic focal fixed dystonia has a physiological or psychologically-mediated mechanism is discussed. CASE REPORT: We report the case of an active 22-year-old soldier with shoulder-fixed dystonia, eight months after a fall with minor right-acromioclavicular sprain. CONCLUSION: Psychiatric examination and search of complex regional pain syndrome, radicular or accessory nerve damage, and genetic predisposition to dystonia are necessary for selecting a difficult treatment in these patients.

[Susac syndrome, retinocochleocerebral microangiopathy: contribution of MRI]. / Le syndrome de Susac, microangiopathie rétinocochléocérébrale : apport de l'IRM.

This is a new case of Susac syndrome in a 27-year-old woman with polymorphic neurological disorders, her brain MRI showed multifocal hyperintense signals on T2-weighted images with possible effects on the corpus callosum. However, visualization of an occlusion in the retinal arterial branch of the right eye and hypoacusia on the right side allowed confirmation of the diagnosis. In this case report, we describe the imaging aspects of Susac syndrome and demonstrate that brain MRI allows the syndrome to be diagnosed at an early stage.

[Syndrome of headache with neurologic deficits and CSF lymphocytosis]. / Syndrome de céphalées et déficits neurologiques transitoires avec lymphocytose du liquide céphalorachidien.

INTRODUCTION: A syndrome of headache with neurologic deficits and cerebrospinal fluid (CSF) lymphocytosis is uncommon and clinicians should be aware of this entity. EXEGESIS: We report a 28-year-old man without previous medical history of migraine, who presented with severe headache and temporary focal, neurological deficits. Lumbar puncture revealed aseptic lymphocytic pleiocytosis. The patient completely recovered within one month. This condition was suggestive of a transient syndrome of headache with neurologic deficits and lymphocytosis. The main characteristics and the pathophysiology of this uncommon disorder, generally with a benign course, are discussed. CONCLUSION: Such syndrome of headache, neurologic deficits and CSF lymphocytosis should be included in the differential diagnosis of meningo-encephalitis. The constant benign course of this affection should be emphasized.

[Reversible acute postpartum cerebral angiopathy]. / Angiopathie cérébrale aiguë réversible du post-partum.

Acute cerebral angiopathy is a rare neuro-vascular complication in postpartum. In this setting, the implication of vasoconstrictive drugs used for lactation or deliverance hemorrhage inhibition has been established. This review aimed 1) to describe, epidemiologic, clinical and diagnostic features of this pathological condition. 2) To put in perspective this condition within the scope of neurovascular clinical syndrome of pregnancy.

[Polyneuropathy involving cranial nerves associated with monoclonal IgM antibodies with anti-MAG/SGPG/SGPLG/sulfatides activity]. / Une polyneuropathie avec atteinte des nerfs crâniens associée à une IgM monoclonale à activité anti-MAG/SGPG/SGPLG/sulfatides.

INTRODUCTION: A typically distal and symmetrical, slowly progressive sensorimotor demyelinating neuropathy is caused by monoclonal IgM against myelin-associated glycoprotein (MAG) and SGPG, SGLPG glycolipids in the context of a benign IgM paraproteinemia. We studied a patient with a neuropathy that fulfilled the diagnostic criteria for CIDP in whom IgM kappa anti-MAG/SGPG/SGLPG were detected. OBSERVATION: The patient was a 57-year-old man who had developed a slowly progressive distal sensorimotor neuropathy, involving the lower then upper limbs, with cranial nerves palsies (oro-pharyngo-laryngo territory). ENMG showed a demyelinating neuropathy with a disproportionate slowing of conduction in distal segments of motor and axonal features in the lower limbs. The first routine laboratory analysis revealed negative or normal findings. Several serum protein electrophoreses were normal. The third cerebrospinal fluid examination demonstrated a moderate and late rise in CSF protein level with no cells. Monoclonal IgM-kappa against MAG/SGPG/SGLPG, was detected; anti-MAG antibody titre in the serum was 20 059 BTU (N<1000). A small IgM-kappa paraprotein was identified by immunofixation. Electron microscopy failed to show nerve fibers with widening of outer lamellae of the myelin. There is no clinical improvement after different treatments, immunoglobulins IV, cortisteroids, plasma exchange, rituximab. CONCLUSION: It is not known whether this neuropathy is an atypical form of PNMAG or an CIDP associated with anti-MAG. When ENMG show a disproportionate slowing of conduction in distal segments of motor nerves, one should screen the serum with immunofixation to identify small monoclonal components. If IgM-MGUS is present, search should be undertaken for anti-MAG/SGPG/SGLPG antibodies. Diagnosis enables optimal treatment using, in severe cases, expensive current strategies with immunoglobulins IV, plasma exchange, and corticosteroids, or, in the event of no response, rituximab before resorting to more toxic drugs like cyclophosphamide.

[Crossed anarthria and a dissociated lateralisation of language]. / Anarthrie croisée et latéralisation dissociée du langage.

INTRODUCTION: Crossed anarthria cases are uncommon and rather old. OBSERVATION: We report the case of a right-handed 55-year-old man who presented crossed pure anarthria due to a hemorrhage in the premotor cortex (feet of F1 and F2) and in the high part of Pierre-Marie's quadrangle. CONCLUSION: The study of different tasks (articulation, verbal fluency, direct object word-generation from a verb) showed a dissociated lateralisation of his language. Lexico-semantic and grammatical tasks are processed in the left hemisphere. Articulation programming occurs in the right hemisphere.

Decreased sympathetic innervation of spleen in aged Fischer 344 rats.

Splenic noradrenergic innervation in young adult and aged Fischer 344 rats was examined using fluorescence histochemistry for catecholamines and high performance liquid chromatography with electrochemical detection (LCEC) for the quantitation of norepinephrine (NE). In young adult rats, abundant noradrenergic plexuses followed the vasculature and trabeculae into splenic white pulp. In aged rats, noradrenergic innervation was reduced in density and in overall intensity of fluorescence, and splenic NE levels were significantly lower. The relationship between diminished noradrenergic innervation and diminished immune responsiveness in aging mammals, while not clear on a causal level, is presented as a hypothesis for further testing.

Chronic dietary pergolide preserves nigrostriatal neuronal integrity in aged-Fischer-344 rats.

Pergolide, a potent D2 presynaptic agonist with postsynaptic D2 agonist activity and some D1 agonist activity was administered in the diet (0.5 mg/kg/day) of male Fischer 344 rats from age 3 to age 26 months. We hypothesized that the potent D2 presynaptic activity would reduce the baseline release of dopamine (DA) and thereby slow the formation of toxic oxidative metabolites that lead to age-related deterioration of nigrostriatal DA neurons. Pair-fed rats served as controls. We observed age-related losses of fluorescent DA cell bodies in the substantia nigra pars compacta and of fluorescent DA terminals in the striatum; chronic pergolide administration prevented these losses. Pergolide administration also prevented the age-related diminution of DA fluorescence intensity in substantia nigra cell bodies. A large decline in 3H-DA uptake with age was partially prevented by pergolide administration. We found no age-related alteration in the concentration of DA in the striatum and pergolide did not alter this concentration. Pergolide treatment resulted in only minor alterations in striatal 3H-spiperone binding and no change in dendritic arborizations of either DA substantia nigra neurons or medium spiny striatal neurons. Pergolide administration also prevented an age-related decline in circulating FSH levels. The uptake data and quantitative morphological findings suggest that pergolide administration in the diet for 2 years exerts a protective effect on age-related deterioration of DA nigrostriatal neurons. This finding was consistent with clinical reports of a subset of patients with Parkinson's disease in whom long-term efficacy of pergolide therapy is observed.

The raphe nuclei of the rabbit brain stem.

The raphe nuclei of the rabbit brain stem were found in the midline and adjacent reticular formation of the medulla, pons, and mesencephalon. Nuclei raphe obscurus, pallidus, and magnus were located in the medulla. Nucleus raphe pontis and the caudal portion of nuclei raphe dorsalis and centralis superior were present in the pons. The rostral portion of nuclei raphe dorsalis and centralis superior, and nuclei linearis caudalis and intermedius were present in the msencephalon. Wings of neurons extended from the midline clusters of raphe neurons into the adjacent reticular formation. These wings of neurons contained serotonergic perikarya which were cytoarchitecturally indistinguishable from the midline neurons. A detailed localization of these nuclei is presented in atlas form. These raphe nuclei contained heterogeneous populations of neurons which varied in the size, shape and density of the cell bodies. In addition, the dendritic branching, specific orientation of dendrites, and appearance of spines were distinct for each of the raphe nuclei. Individual raphe nuclei often contained several subpopulations of neurons characterized by unique spatial configuration and orientation. The main morphological similarities of the raphe nuclei are location in or adjacent to the midline, the presence of serotonergic cell bodies in all raphe nuclei except the linear nuclei, and heterogeneous cell populations.

A raphe dendrite bundle in the rabbit medulla.

A Golgi-Cox, histofluorescence, and electron microscopic examination of the serotonergic raphe nuclei of the rabbit medulla has revealed a large, vertically-oriented midline dendrite bundle extending from the floor of the fourth ventricle to the ventral boundary of nucleus raphe pallidus. The bundle was confined to the medulla, and averaged 150-200 micrometer in width in the adult. This dendrite bundle received contributions from four major sources: (1) Dendrites of midline and paramedian neurons of nucleus raphe obscurus; (2) Dendrites of midline and paramedian neurons of nucleus raphe pallidus; (3) Shafts from tanycytes located on the midline floor of the fourth ventricle; and (4) Dendrites from neurons of the medullary reticular formation. Perikarya and dendrites of serotonergic raphe neurons frequently abutted tanycyte shafts, midline bhood vessels, and perikarya and dendrites of other raphe neurons. The tanycyte shafts extended from the floor of the fourth ventricle into the bundle, and often ran the entire length of the bundle, where they intertwined themselves among neurons and dendrites of the medullary raphe nuclei. This study suggests that neurons of the medullary raphe may be influenced by communication channels including dendro-dendritic contacts within the midline bundle, fourth ventricular cerebrospinal fluid-borne influences through tanycyte shafts, blood-borne influences through the direct neuronal-vascular relationship in the raphe, and traditionally described axonal contacts impinging upon raphe neurons. We suggest that the raphe neurons might act as both neurons and endocrine-neural transducer cells.

Viscerotopic localization of preganglionic parasympathetic cell bodies of origin of the anterior and posterior subdiaphragmatic vagus nerves.

Utilizing the retrograde HRP transport method, fibers from anterior and posterior subdiaphragmatic branches of the vagus nerve in the rat were traced to their cells of origin in the brainstem. Efferents to the gut supplied by the subdiaphragmatic vagus nerves derive from cell bodies organized in a viscerotopic, spindle-shaped longitudinal cell column throughout the longitudinal extent of the classically described dorsal nucleus of the vagus (DNV) and in regions of nucleus commissuralis (NC), caudal to the DNV. This entire longitudinal group of cells is called the DNV cell column. In the caudal one third of the DNV cell column, the cell bodies were found in the midline and paramedian posterior portion of the NC, and in the anterior portion of the caudal DNV, in a horizontally oriented cluster of cells when viewed in cross section. In the middle one third of the DNV cell column, the cell bodies moved laterally, but still maintained their anterior position in the nucleus. In the rostral one third of the cell column, the cell bodies were located at the lateral margin of the DNV. A few scattered cell bodies extended caudally from the DNV cell column into the dorsal region of lamina X of spinal cord, and reached as far caudal as the C5-C6 segments. The anterior subdiaphragmatic branch of the vagus contained axons whose cell bodies were mainly but not exclusively located in the ipsilateral (left) side of the medulla, while the posterior subdiaphragmatic branch of the vagus contained axons whose cell bodies were found bilaterally in the medulla, with a majority (approx. 60%) located on the ipsilateral (right) side, and approximately 40% located on the contralateral (left) side.

Alterations in sympathetic innervation of thymus and spleen in aged mice.

Age is associated with reduced immune reactivity, contributing to increased rates of infectious disease and cancer in old age. We have begun to assess the potential for sympathetic nervous system involvement in age-related immune dysfunction by characterizing sympathetic noradrenergic (NA) innervation in lymphoid organs in old animals. In the present study noradrenergic innervation of spleen and thymus was examined histologically and neurochemically in 2-, 12- and 24-month old BALB/c mice. In the thymus of 2-month old animals, NA nerve fibers were found in the subcapsular, cortical, and cortico-medullary regions associated with blood vessels and septa; occasional branches from these nerve fibers entered the parenchyma. With increasing age and thymic involution, NA nerve fibers increased in density; by 24 months of age, dense plexuses were compacted among septa and blood vessels, and numerous linear, varicose nerve fibers were observed branching into the parenchyma. Thymic norepinephrine (NE) concentration (per mg wet weight) increased approximately 4-fold in 12-month old animals and 15-fold in 24-month old animals. Taking the reduced thymus weight into account, total thymic NE at 12- and 24-month of age was equivalent to total thymic NE at 2-month of age, suggesting that NA innervation is maintained as the thymus involutes. In the spleen from 2-month old animals, NA innervation entered the white pulp with the central artery to innervate the periarteriolar lymphatic sheath and the marginal zone. At 12-month of age, histologically and neurochemically there was no change in splenic NA innervation. By 24-month of age, NE was increased significantly, independent of changes in spleen weight. Histologically, increased catecholamine-containing fibers were apparent at 24-month of age, particularly in the parenchyma surrounding the central artery. The alterations in sympathetic NA innervation of lymphoid organs with age suggest that the sympathetic nervous system and NE may play a role in age-associated immune dysregulation. Alternatively, the changes in NA innervation may be secondary to functional changes within the immune system.

Restoration of sympathetic noradrenergic nerve fibers in the spleen by low doses of L-deprenyl treatment in young sympathectomized and old Fischer 344 rats.

It is well-established that noradrenergic (NA) nerve fibers in spleen and lymph nodes influence cell-mediated immune responses. Such responses are diminished in young animals following chemical sympathectomy and in older animals accompanying an age-related decline in NA nerve fibers in spleen and lymph nodes. The purpose of this study was to determine whether treatment with deprenyl, an irreversible monoamine oxidase-B (MAO-B) inhibitor, would hasten the process of splenic NA reinnervation following chemical sympathectomy in young rats and would reverse the age-related loss of sympathetic NA fibers in the spleen of old rats. To examine the effects of deprenyl in young sympathectomized rats, 3-month-old male Fischer 344 (F344) rats were treated with 6-hydroxydopamine (6-OHDA) and administered 0, 0.25, 1.0, 2.5, or 5.0 mg deprenyl/kg body weight (BW)/day intraperitoneally (i.p.) for 1, 15, or 30 days. In another study, 21-month-old male F344 rats were treated with 0, 0.25, or 1.0 mg deprenyl/kg BW/day i.p. for 9 weeks. At the end of the treatment period, spleens were removed and NA innervation was assessed by fluorescence histochemistry, immunocytochemistry, and quantitation of norepinephrine (NE) by high performance liquid chromatography with electrochemical detection (HPLC-EC). In the spleens of young sympathectomized rats, there was faint fluorescence or absence of fluorescence and tyrosine hydroxylase-positive (TH+) fibers around the central arteriole and in the periarteriolar lymphatic sheath of the white pulp one day after administration of 6-OHDA, indicating a severe loss of NA innervation compared with unlesioned control animals. Treatment of sympathectomized rats with 1.0 mg, 2.5 mg, and 5.0 mg/kg deprenyl for 30 days increased the density of NA innervation estimated by both fluorescence histochemistry and immunocytochemistry compared with vehicle-treated controls recovering spontaneously from 6-OHDA. Splenic NE concentration was increased in the hilar region of sympathectomized rats treated with 2.5 mg and 1.0 mg/kg deprenyl after 15 and 30 days, respectively, compared with untreated and vehicle-treated sympathectomized rats. The spleens of untreated and saline-treated old rats showed a reduction in the density of NA innervation in the white pulp compared with young animals. Treatment of old rats for 9 weeks with 1.0 mg/kg deprenyl induced moderate to intense fluorescent fibers and linear TH+ nerve fibers around the central arteriole and in other compartments of the white pulp, and increased splenic NE concentration in the hilar region and NE content in the whole spleen. Taken together, these results provide strong evidence for a neurorestorative property of deprenyl on sympathetic NA innervation of the spleen, which may lead to an improvement in cell-mediated immune responses.

Corticosterone responses of adult Lewis and Fischer rats.

Indwelling catheters were implanted into the inferior vena cava of adult male and female Lewis/N and Fischer 344 rats. Each animal was exposed to ACTH, novelty stimulation, nicotine, lipopolysaccharide (LPS), and saline on 5 consecutive days. Blood was withdrawn before (baseline) and at several time points after the stimulus on each day. There were no differences in baseline corticosterone levels nor in responses to saline in any group. In general, responses to stimulation peaked at 15-30 min and returned to baseline by 60-90 min. Corticosterone responses to LPS showed a different time course; maximal responses occur at 1-2 h and return to baseline by 24 h. Fischer animals showed higher corticosterone levels than Lewis rats during the response to stimulation, but returned to baseline at the same times. Females of each strain showed higher corticosterone responses than males at 15, 30, and 45 min after ACTH, but the sexes did not differ in response to the other stimuli. For individual rats, the maximum response to ACTH was slightly correlated with the maximum response to novelty stimulation, nicotine, and saline but was not correlated with the response to LPS.

Effects of L-deprenyl treatment on noradrenergic innervation and immune reactivity in lymphoid organs of young F344 rats.

Sympathetic noradrenergic (NA) neuronal activities in the thymus, spleen and mesenteric lymph nodes (MLN) and immune responses in the spleen were examined in young male F344 rats treated daily with 0, 0.25 mg, or 2.5 mg/kg body weight of L-deprenyl, an irreversible monoamine oxidase-B (MAO-B) inhibitor. Rats were treated daily for 1, 15, or 30 days, and sacrificed 7 days after the last deprenyl treatment. Deprenyl treatment increased norepinephrine (NE) content in the spleen without modifying the pattern and density of NA innervation in the splenic white pulp. The concentration of NE was unaltered in the thymus, but it was increased in the MLN of deprenyl-treated rats. One day of treatment with deprenyl decreased splenic NK cell activity while 15 days of deprenyl treatment enhanced splenic NK cell activity. Deprenyl elevated Con A-induced T lymphocyte proliferation following 30 days of treatment, but did not alter spleen cell Con A-induced IL-2 production or the percentage of CD5 + T cells in the spleen. A moderate decrease in the percentage of sIgM + B cells was observed in the spleens of 15- and 30-day deprenyl-treated rats. These results suggest that deprenyl has sympathomimetic action on sympathetic NA nerve fibers in the spleen; the enhancement of NA neuronal activity may contribute to the modulation of immune responses in the spleen.

Effects of interleukin-2 on the expression of corticotropin-releasing hormone in nerves and lymphoid cells in secondary lymphoid organs from the Fischer 344 rat.

This study examined the influence of interleukin (IL)-2 on corticotropin releasing hormone (CRH) immunoreactivity in the Fischer 344 (F344) rat spleen. Rats were given either vehicle or 1, 10, 25, 50, 100, or 200 ng of human recombinant (hr)IL-2 by intraperitoneal (i.p.) injection, and were sacrificed 0.5, 1, 4, 12, or 24 h after treatment. Spleens and mesenteric lymph nodes were prepared for immunocytochemistry to localize CRH. In spleens from vehicle-treated animals, CRH immunoreactivity was present in several types of cells of the immune system, but CRH(+) nerves were not observed in either spleens or lymph nodes from vehicle-treated animals. Treatment with IL-2 induced CRH expression in nerves in the spleen in a dose- and time-dependent manner. CRH(+) nerves were not found in the mesenteric lymph nodes after IL-2 treatment, instead a dramatic time- and dose-dependent accumulation of CRH(+) cells (resembling small lymphocytes and large granular mononuclear cells) in the cortex and medulla. These findings indicate that IL-2 stimulates the synthesis of CRH in nerves that innervate the F344 rat spleen, and promote the appearance of CRH(+) immunocytes into draining mesenteric lymph nodes.

Anti-tumor effect of L-deprenyl is associated with enhanced central and peripheral neurotransmission and immune reactivity in rats with carcinogen-induced mammary tumors.

L-Deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, has previously been shown to improve immune responses and restore noradrenergic (NA) nerve fibers in the spleen of old rats. In tumor-bearing rats, L-deprenyl inhibited tumor incidence and enhanced tuberoinfundibular dopaminergic (TIDA) neurotransmission in the hypothalamus. The aim of the present study was to investigate whether alterations in sympathetic NA activity and cellular immune responses in the spleen, and TIDA activity in the hypothalamus, accompany deprenyl-induced regression of 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced mammary tumors. Rats with DMBA-induced mammary tumors were treated with 0, 2.5 mg, or 5.0 mg/kg body weight of deprenyl daily for 13 weeks. Saline-treated tumor-bearing rats exhibited reduced splenic IL-2 and IFN-gamma levels, and lowered splenic norepinephrine (NE) concentration and hypothalamic dopaminergic activity, compared to rats without tumors. In contrast, treatment with 2.5 mg/kg and 5.0 mg/kg of deprenyl reduced the number and size of mammary tumors. Deprenyl-induced tumor regression was accompanied by increased immune measures in the spleen, including enhanced IL-2 and IFN-gamma production, and NK cell activity. Neural measures enhanced by deprenyl included NE concentration in the spleen and TIDA neuronal activity in the hypothalamus. These results suggest that (1) mammary tumorigenesis is associated with the inhibition of sympathetic NA activity in the spleen, TIDA activity in the hypothalamus, and cell-mediated immunity, and (2) reversal of the inhibition of catecholaminergic neuronal activities of the central nervous system and peripheral nervous system by deprenyl may enhance anti-tumor immunity.