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Narcolepsy is the most common neurological cause of chronic sleepiness. The discovery about 20 years ago that narcolepsy is caused by selective loss of the neurons producing orexins (also known as hypocretins) sparked great advances in the field. Here, we review the current understanding of how orexin neurons regulate sleep–wake behaviour and the consequences of the loss of orexin neurons. We also summarize the developing evidence that narcolepsy is an autoimmune disorder that may be caused by a T cell-mediated attack on the orexin neurons and explain how these new perspectives can inform better therapeutic approaches.
Silber, M. H., Krahn, L. E., Olson, E. J. & Pankratz, V. S. The epidemiology of narcolepsy in Olmsted County, Minnesota: a population-based study. Sleep 25, 197–202 (2002).
Shin, Y. K. et al. Prevalence of narcolepsy-cataplexy in Korean adolescents. Acta Neurol. Scand. 117, 273–278 (2008).
Longstreth, W. T. Jr. et al. Prevalence of narcolepsy in King County, WA, USA. Sleep Med. 10, 422–426 (2009).
Knudsen, S., Gammeltoft, S. & Jennum, P. J. Rapid eye movement sleep behaviour disorder in patients with narcolepsy is associated with hypocretin-1 deficiency. Brain 133, 568–579 (2010).
de Lecea, L. et al. The hypocretins: hypothalamus-specific peptides with neuroexcitatory activity. Proc. Natl Acad. Sci. USA 95, 322–327 (1998). This paper is one of the first descriptions of the orexin neuropeptides (naming them hypocretins).
Sakurai, T. et al. Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior. Cell 92, 573–585 (1998). This article is one of the first to describe the orexin neuropeptides.
Peyron, C. et al. A mutation in a case of early onset narcolepsy and a generalized absence of hypocretin peptides in human narcoleptic brains. Nat. Med. 6, 991–997 (2000). This paper highlights the discovery of a lack of orexin in the brains of people with narcolepsy.
Thannickal, T. C. et al. Reduced number of hypocretin neurons in human narcolepsy. Neuron 27, 469–474 (2000). This study also shows a lack of orexin in the brains of people with narcolepsy.
Crocker, A. et al. Concomitant loss of dynorphin, NARP, and orexin in narcolepsy. Neurology 65, 1184–1188 (2005). This paper demonstrates that orexin neurons co-express dynorphin and NARP and that narcolepsy is due to a loss of the orexin neurons, not just a reduction in orexin expression.
American Academy of Sleep Medicine. International Classification of Sleep Disorders 3rd edn (AASM, 2014).
Thannickal, T. C., Nienhuis, R. & Siegel, J. M. Localized loss of hypocretin (orexin) cells in narcolepsy without cataplexy. Sleep 32, 993–998 (2009). This paper shows that NT2 may be caused by partial loss of the orexin neurons.
Tabuchi, S. et al. Conditional ablation of orexin/hypocretin neurons: a new mouse model for the study of narcolepsy and orexin system function. J. Neurosci. 34, 6495–6509 (2014).
Kanbayashi, T. et al. The pathophysiologic basis of secondary narcolepsy and hypersomnia. Curr. Neurol. Neurosci. Rep. 11, 235–241 (2011).
Hor, H. et al. A missense mutation in myelin oligodendrocyte glycoprotein as a cause of familial narcolepsy with cataplexy. Am. J. Hum. Genet. 89, 474–479 (2011).
Andlauer, O. et al. Predictors of hypocretin (orexin) deficiency in narcolepsy without cataplexy. Sleep 35, 1247–1255 (2012).
Luca, G. et al. Clinical, polysomnographic and genome-wide association analyses of narcolepsy with cataplexy: a European Narcolepsy Network study. J. Sleep Res. 22, 482–495 (2013).
Lopez, R. et al. Temporal changes in the cerebrospinal fluid level of hypocretin-1 and histamine in narcolepsy. Sleep 40, zsw010 (2017).
Pizza, F. et al. Primary progressive narcolepsy type 1: the other side of the coin. Neurology 83, 2189–2190 (2014).
Peyron, C. et al. Neurons containing hypocretin (orexin) project to multiple neuronal systems. J. Neurosci. 18, 9996–10015 (1998). This study thoroughly describes the projections of the orexin neurons.
Gonzalez, J. A., Iordanidou, P., Strom, M., Adamantidis, A. & Burdakov, D. Awake dynamics and brain-wide direct inputs of hypothalamic MCH and orexin networks. Nat. Commun. 7, 11395 (2016).
van den Pol, A. N. Hypothalamic hypocretin (orexin): robust innervation of the spinal cord. J. Neurosci. 19, 3171–3182 (1999).
Sakurai, T. et al. Input of orexin/hypocretin neurons revealed by a genetically encoded tracer in mice. Neuron 46, 297–308 (2005).
Mieda, M. et al. Differential roles of orexin receptor-1 and -2 in the regulation of non-REM and REM sleep. J. Neurosci. 31, 6518–6526 (2011).
Kantor, S. et al. Orexin neurons are necessary for the circadian control of REM sleep. Sleep 32, 1127–1134 (2009).
Lee, M. G., Hassani, O. K. & Jones, B. E. Discharge of identified orexin/hypocretin neurons across the sleep-waking cycle. J. Neurosci. 25, 6716–6720 (2005). This paper describes the firing pattern of orexin neurons across different sleep–wake states.
Mileykovskiy, B. Y., Kiyashchenko, L. I. & Siegel, J. M. Behavioral correlates of activity in identified hypocretin/orexin neurons. Neuron 46, 787–798 (2005). This study highlights increased activity in the orexin neurons during exploratory behaviour and wake.
Estabrooke, I. V. et al. Fos expression in orexin neurons varies with behavioral state. J. Neurosci. 21, 1656–1662 (2001).
España, R. A., Valentino, R. J. & Berridge, C. W. Fos immunoreactivity in hypocretin-synthesizing and hypocretin-1 receptor-expressing neurons: effects of diurnal and nocturnal spontaneous waking, stress and hypocretin-1 administration. Neuroscience 121, 201–217 (2003).
Adamantidis, A. R., Zhang, F., Aravanis, A. M., Deisseroth, K. & de Lecea, L. Neural substrates of awakening probed with optogenetic control of hypocretin neurons. Nature 450, 420–424 (2007). This study is the first demonstration that photostimulation of the orexin neurons promotes waking from sleep.
Tsunematsu, T. et al. Long-lasting silencing of orexin/hypocretin neurons using archaerhodopsin induces slow-wave sleep in mice. Behav. Brain Res. 255, 64–74 (2013).
Sasaki, K. et al. Pharmacogenetic modulation of orexin neurons alters sleep/wakefulness states in mice. PLOS ONE 6, e20360 (2011).
Mieda, M. et al. Orexin peptides prevent cataplexy and improve wakefulness in an orexin neuron-ablated model of narcolepsy in mice. Proc. Natl Acad. Sci. USA 101, 4649–4654 (2004).
Irukayama-Tomobe, Y. et al. Nonpeptide orexin type-2 receptor agonist ameliorates narcolepsy-cataplexy symptoms in mouse models. Proc. Natl Acad. Sci. USA 114, 5731–5736 (2017).
Suntsova, N. et al. The median preoptic nucleus reciprocally modulates activity of arousal-related and sleep-related neurons in the perifornical lateral hypothalamus. J. Neurosci. 27, 1616–1630 (2007).
Uschakov, A., Gong, H., McGinty, D. & Szymusiak, R. Efferent projections from the median preoptic nucleus to sleep- and arousal-regulatory nuclei in the rat brain. Neuroscience 150, 104–120 (2007).
Li, Y., Gao, X. B., Sakurai, T. & van den Pol, A. N. Hypocretin/orexin excites hypocretin neurons via a local glutamate neuron — a potential mechanism for orchestrating the hypothalamic arousal system. Neuron 36, 1169–1181 (2002).
Yamanaka, A., Tabuchi, S., Tsunematsu, T., Fukazawa, Y. & Tominaga, M. Orexin directly excites orexin neurons through orexin 2 receptor. J. Neurosci. 30, 12642–12652 (2010).
Vassalli, A., Li, S. & Tafti, M. Comment on “Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor 2”. Sci. Transl Med. 7, 314le2 (2015).
Schone, C., Apergis-Schoute, J., Sakurai, T., Adamantidis, A. & Burdakov, D. Coreleased orexin and glutamate evoke nonredundant spike outputs and computations in histamine neurons. Cell Rep. 7, 697–704 (2014).
Herring, W. J. et al. Orexin receptor antagonism for treatment of insomnia: a randomized clinical trial of suvorexant. Neurology 79, 2265–2274 (2012).
Svetnik, V. et al. Insight into reduction of wakefulness by suvorexant in patients with insomnia: analysis of wake bouts. Sleep 41, zsx178 (2018).
Schone, C. & Burdakov, D. Glutamate and GABA as rapid effectors of hypothalamic “peptidergic” neurons. Front. Behav. Neurosci. 6, 81 (2012).
Kosse, C., Schone, C., Bracey, E. & Burdakov, D. Orexin-driven GAD65 network of the lateral hypothalamus sets physical activity in mice. Proc. Natl Acad. Sci. USA 114, 4525–4530 (2017).
Chang, M. C. et al. Narp regulates homeostatic scaling of excitatory synapses on parvalbumin-expressing interneurons. Nat. Neurosci. 13, 1090–1097 (2010).
Reti, I. M., Reddy, R., Worley, P. F. & Baraban, J. M. Selective expression of Narp, a secreted neuronal pentraxin, in orexin neurons. J. Neurochem. 82, 1561–1565 (2002).
Blouin, A. M. et al. Narp immunostaining of human hypocretin (orexin) neurons: loss in narcolepsy. Neurology 65, 1189–1192 (2005).
Chou, T. C. et al. Orexin (hypocretin) neurons contain dynorphin. J. Neurosci. 21, RC168 (2001).
Muschamp, J. W. et al. Hypocretin (orexin) facilitates reward by attenuating the antireward effects of its cotransmitter dynorphin in ventral tegmental area. Proc. Natl Acad. Sci. USA 111, E1648–E1655 (2014).
Ferrari, L. L. et al. Regulation of lateral hypothalamic orexin activity by local GABAergic neurons. J. Neurosci. 38, 1588–1599 (2018).
Baimel, C., Lau, B. K., Qiao, M. & Borgland, S. L. Projection-target-defined effects of orexin and dynorphin on VTA dopamine neurons. Cell Rep. 18, 1346–1355 (2017). This paper shows that the effects of orexin and dynorphin vary across VTA neurons that innervate different targets.
Narita, M. et al. Direct involvement of orexinergic systems in the activation of the mesolimbic dopamine pathway and related behaviors induced by morphine. J. Neurosci. 26, 398–405 (2006).
Aston-Jones, G., Smith, R. J., Moorman, D. E. & Richardson, K. A. Role of lateral hypothalamic orexin neurons in reward processing and addiction. Neuropharmacology 56 (Suppl. 1), 112–121 (2009).
Harris, G. C. & Aston-Jones, G. Arousal and reward: a dichotomy in orexin function. Trends Neurosci. 29, 571–577 (2006).
Smith, R. J., Tahsili-Fahadan, P. & Aston-Jones, G. Orexin/hypocretin is necessary for context-driven cocaine-seeking. Neuropharmacology 58, 179–184 (2010).
Beig, M. I., Dampney, B. W. & Carrive, P. Both Ox1r and Ox2r orexin receptors contribute to the cardiovascular and locomotor components of the novelty stress response in the rat. Neuropharmacology 89, 146–156 (2015).
Ciriello, J. & de Oliveira, C. V. Cardiac effects of hypocretin-1 in nucleus ambiguus. Am. J. Physiol. Regul. Integr. Comp. Physiol. 284, R1611–R1620 (2003).
Ciriello, J., Li, Z. & de Oliveira, C. V. Cardioacceleratory responses to hypocretin-1 injections into rostral ventromedial medulla. Brain Res. 991, 84–95 (2003).
Shirasaka, T., Nakazato, M., Matsukura, S., Takasaki, M. & Kannan, H. Sympathetic and cardiovascular actions of orexins in conscious rats. Am. J. Physiol. 277, R1780–R1785 (1999).
Li, A., Hindmarch, C. C., Nattie, E. E. & Paton, J. F. Antagonism of orexin receptors significantly lowers blood pressure in spontaneously hypertensive rats. J. Physiol. 591, 4237–4248 (2013).
Mohammed, M., Ootsuka, Y., Yanagisawa, M. & Blessing, W. Reduced brown adipose tissue thermogenesis during environmental interactions in transgenic rats with ataxin-3-mediated ablation of hypothalamic orexin neurons. Am. J. Physiol. Regul. Integr. Comp. Physiol. 307, R978–R989 (2014).
Lubkin, M. & Stricker-Krongrad, A. Independent feeding and metabolic actions of orexins in mice. Biochem. Biophys. Res. Commun. 253, 241–245 (1998).
Hansen, M. H., Kornum, B. R. & Jennum, P. Sleep-wake stability in narcolepsy patients with normal, low and unmeasurable hypocretin levels. Sleep Med. 34, 1–6 (2017).
Littner, M. R. et al. Practice parameters for clinical use of the multiple sleep latency test and the maintenance of wakefulness test. Sleep 28, 113–121 (2005).
Chemelli, R. M. et al. Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation. Cell 98, 437–451 (1999). This paper provides the first evidence that loss of orexin signalling in mice produces sleepiness and cataplexy.
Hara, J. et al. Genetic ablation of orexin neurons in mice results in narcolepsy, hypophagia, and obesity. Neuron 30, 345–354 (2001).
Mochizuki, T. et al. Behavioral state instability in orexin knock-out mice. J. Neurosci. 24, 6291–6300 (2004).
Mochizuki, T. et al. Orexin receptor 2 expression in the posterior hypothalamus rescues sleepiness in narcoleptic mice. Proc. Natl Acad. Sci. USA 108, 4471–4476 (2011).
Branch, A. F. et al. Progressive loss of the orexin neurons reveals dual effects on wakefulness. Sleep 39, 369–377 (2016).
Vassalli, A. & Franken, P. Hypocretin (orexin) is critical in sustaining theta/gamma-rich waking behaviors that drive sleep need. Proc. Natl Acad. Sci. USA 114, E5464–E5473 (2017).
Diniz Behn, C. G., Klerman, E. B., Mochizuki, T., Lin, S. C. & Scammell, T. E. Abnormal sleep/wake dynamics in orexin knockout mice. Sleep 33, 297–306 (2010).
España, R. A., Baldo, B. A., Kelley, A. E. & Berridge, C. W. Wake-promoting and sleep-suppressing actions of hypocretin (orexin): basal forebrain sites of action. Neuroscience 106, 699–715 (2001).
Hasegawa, E., Yanagisawa, M., Sakurai, T. & Mieda, M. Orexin neurons suppress narcolepsy via 2 distinct efferent pathways. J. Clin. Invest. 124, 604–616 (2014).
Carter, M. E. et al. Mechanism for hypocretin-mediated sleep-to-wake transitions. Proc. Natl Acad. Sci. USA 109, E2635–E2644 (2012).
Roman, A., Meftah, S., Arthaud, S., Luppi, P. H. & Peyron, C. The inappropriate occurrence of rapid eye movement sleep in narcolepsy is not due to a defect in homeostatic regulation of rapid eye movement sleep. Sleep 41, zsy046 (2018).
Andlauer, O. et al. Nocturnal rapid eye movement sleep latency for identifying patients with narcolepsy/hypocretin deficiency. JAMA Neurol. 70, 891–902 (2013).
Reiter, J., Katz, E., Scammell, T. E. & Maski, K. Usefulness of a nocturnal SOREMP for diagnosing narcolepsy with cataplexy in a pediatric population. Sleep 38, 859–865 (2015).
Tafti, M., Villemin, E., Carlander, B., Besset, A. & Billiard, M. Sleep onset rapid-eye-movement episodes in narcolepsy: REM sleep pressure or nonREM–REM sleep dysregulation? J. Sleep Res. 1, 245–250 (1992).
Dantz, B., Edgar, D. M. & Dement, W. C. Circadian rhythms in narcolepsy: studies on a 90 minute day. Electroencephalogr. Clin. Neurophysiol. 90, 24–35 (1994).
Chen, K. S. et al. A hypothalamic switch for REM and non-REM sleep. Neuron 97, 1168–1176 (2018).
España, R. A., McCormack, S. L., Mochizuki, T. & Scammell, T. E. Running promotes wakefulness and increases cataplexy in orexin knockout mice. Sleep 30, 1417–1425 (2007).
Kaur, S. et al. Hypocretin-2 saporin lesions of the ventrolateral periaquaductal gray (vlPAG) increase REM sleep in hypocretin knockout mice. PLOS ONE 4, e6346 (2009).
Luppi, P. H. et al. Paradoxical (REM) sleep genesis: |the switch from an aminergic-cholinergic to a GABAergic-glutamatergic hypothesis. J. Physiol. Paris 100, 271–283 (2006).
Luppi, P. H. et al. Brainstem mechanisms of paradoxical (REM) sleep generation. Pflugers Arch. 463, 43–52 (2012).
Burgess, C. R., Oishi, Y., Mochizuki, T., Peever, J. H. & Scammell, T. E. Amygdala lesions reduce cataplexy in orexin knock-out mice. J. Neurosci. 33, 9734–9742 (2013).
Mahoney, C. E., Agostinelli, L. J., Brooks, J. N., Lowell, B. B. & Scammell, T. E. GABAergic neurons of the central amygdala promote cataplexy. J. Neurosci. 37, 3995–4006 (2017). This paper demonstrates that the central amygdala is necessary for emotion-triggered cataplexy.
Snow, M. B. et al. GABA cells in the central nucleus of the amygdala promote cataplexy. J. Neurosci. 37, 4007–4022 (2017).
Hasegawa, E. et al. Serotonin neurons in the dorsal raphe mediate the anticataplectic action of orexin neurons by reducing amygdala activity. Proc. Natl Acad. Sci. USA 114, E3526–E3535 (2017).
Broughton, R. et al. Excessive daytime sleepiness and the pathophysiology of narcolepsy-cataplexy: a laboratory perspective. Sleep 9, 205–215 (1986).
Schoch, S. F. et al. Dysregulation of sleep behavioral states in narcolepsy. Sleep 40, zsx170 (2017).
Ponziani, V. et al. Growing up with type 1 narcolepsy: its anthropometric and endocrine features. J. Clin. Sleep Med. 12, 1649–1657 (2016).
Lammers, G. J. et al. Spontaneous food choice in narcolepsy. Sleep 19, 75–76 (1996).
Nishino, S. et al. Low cerebrospinal fluid hypocretin (orexin) and altered energy homeostasis in human narcolepsy. Ann. Neurol. 50, 381–388 (2001).
Poli, F. et al. High prevalence of precocious puberty and obesity in childhood narcolepsy with cataplexy. Sleep 36, 175–181 (2013).
Wang, Z. et al. Body weight and basal metabolic rate in childhood narcolepsy: a longitudinal study. Sleep Med. 25, 139–144 (2016).
van Holst, R. J. et al. Aberrant food choices after satiation in human orexin-deficient narcolepsy type 1. Sleep 39, 1951–1959 (2016).
Dimitrova, A. et al. Reward-seeking behavior in human narcolepsy. J. Clin. Sleep Med. 7, 293–300 (2011).
Zhang, S., Zeitzer, J. M., Sakurai, T., Nishino, S. & Mignot, E. Sleep/wake fragmentation disrupts metabolism in a mouse model of narcolepsy. J. Physiol. 581, 649–663 (2007). This paper demonstrates that resting metabolic rate is reduced in mice lacking orexin neurons.
Fronczek, R. et al. Increased heart rate variability but normal resting metabolic rate in hypocretin/orexin-deficient human narcolepsy. J. Clin. Sleep Med. 4, 248–254 (2008).
Dahmen, N., Tonn, P., Messroghli, L., Ghezel-Ahmadi, D. & Engel, A. Basal metabolic rate in narcoleptic patients. Sleep 32, 962–964 (2009).
Chabas, D. et al. Eating disorder and metabolism in narcoleptic patients. Sleep 30, 1267–1273 (2007).
Donjacour, C. E. et al. Glucose and fat metabolism in narcolepsy and the effect of sodium oxybate: a hyperinsulinemic-euglycemic clamp study. Sleep 37, 795–801 (2014).
Maurovich-Horvat, E. et al. Hypothalamo-pituitary-adrenal axis, glucose metabolism and TNF-α in narcolepsy. J. Sleep Res. 23, 425–431 (2014).
Poli, F. et al. Body mass index-independent metabolic alterations in narcolepsy with cataplexy. Sleep 32, 1491–1497 (2009).
Hutcheson, D. M. et al. Orexin-1 receptor antagonist SB-334867 reduces the acquisition and expression of cocaine-conditioned reinforcement and the expression of amphetamine-conditioned reward. Behav. Pharmacol. 22, 173–181 (2011).
Sartor, G. C. & Aston-Jones, G. S. A septal-hypothalamic pathway drives orexin neurons, which is necessary for conditioned cocaine preference. J. Neurosci. 32, 4623–4631 (2012).
Plaza-Zabala, A., Flores, A., Maldonado, R. & Berrendero, F. Hypocretin/orexin signaling in the hypothalamic paraventricular nucleus is essential for the expression of nicotine withdrawal. Biol. Psychiatry 71, 214–223 (2012).
Plaza-Zabala, A., Martin-Garcia, E., de Lecea, L., Maldonado, R. & Berrendero, F. Hypocretins regulate the anxiogenic-like effects of nicotine and induce reinstatement of nicotine-seeking behavior. J. Neurosci. 30, 2300–2310 (2010).
Georgescu, D. et al. Involvement of the lateral hypothalamic peptide orexin in morphine dependence and withdrawal. J. Neurosci. 23, 3106–3111 (2003).
Sharf, R., Sarhan, M. & Dileone, R. J. Orexin mediates the expression of precipitated morphine withdrawal and concurrent activation of the nucleus accumbens shell. Biol. Psychiatry 64, 175–183 (2008).
Shoblock, J. R. et al. Selective blockade of the orexin-2 receptor attenuates ethanol self-administration, place preference, and reinstatement. Psychopharmacology 215, 191–203 (2011).
Sharf, R., Guarnieri, D. J., Taylor, J. R. & DiLeone, R. J. Orexin mediates morphine place preference, but not morphine-induced hyperactivity or sensitization. Brain Res. 1317, 24–32 (2010).
Riday, T. T. et al. Orexin-1 receptor antagonism does not reduce the rewarding potency of cocaine in Swiss-Webster mice. Brain Res. 1431, 53–61 (2012).
Voorhees, C. M. & Cunningham, C. L. Involvement of the orexin/hypocretin system in ethanol conditioned place preference. Psychopharmacology 214, 805–818 (2011).
Bayard, S., Langenier, M. C. & Dauvilliers, Y. Decision-making, reward-seeking behaviors and dopamine agonist therapy in restless legs syndrome. Sleep 36, 1501–1507 (2013).
Barateau, L. et al. Smoking, alcohol, drug use, abuse and dependence in narcolepsy and idiopathic hypersomnia: a case-control study. Sleep 39, 573–580 (2016).
Cohen, A., Mandrekar, J., St Louis, E. K., Silber, M. H. & Kotagal, S. Comorbidities in a community sample of narcolepsy. Sleep Med. 43, 14–18 (2018).
Lee, M. J. et al. Comorbidity of narcolepsy and depressive disorders: a nationwide population-based study in Taiwan. Sleep Med. 39, 95–100 (2017).
Inocente, C. O. et al. Depressive feelings in children with narcolepsy. Sleep Med. 15, 309–314 (2014).
Lopez, R., Barateau, L., Evangelista, E. & Dauvilliers, Y. Depression and hypersomnia: a complex association. Sleep Med. Clin. 12, 395–405 (2017).
Chastain, E. M., Duncan, D. S., Rodgers, J. M. & Miller, S. D. The role of antigen presenting cells in multiple sclerosis. Biochim. Biophys. Acta 1812, 265–274 (2011).
Yong, V. W. & Antel, J. P. Major histocompatibility complex molecules on glial cells. Semin. Neurosci. 4, 231–240 (1992).
Wuthrich, C., Batson, S. & Koralnik, I. J. Lack of major histocompatibility complex class I upregulation and restrictive infection by JC virus hamper detection of neurons by T lymphocytes in the central nervous system. J. Neuropathol. Exp. Neurol. 74, 791–803 (2015).
Clarkson, B. D. S., Patel, M. S., LaFrance-Corey, R. G. & Howe, C. L. Retrograde interferon-gamma signaling induces major histocompatibility class I expression in human-induced pluripotent stem cell-derived neurons. Ann. Clin. Transl Neurol. 5, 172–185 (2018).
Zhang, A. et al. Developmental expression and localization of MHC class I molecules in the human central nervous system. Exp. Brain Res. 233, 2733–2743 (2015).
Partinen, M. et al. Increased incidence and clinical picture of childhood narcolepsy following the 2009 H1N1 pandemic vaccination campaign in Finland. PLOS ONE 7, e33723 (2012). This paper describes the increased incidence of narcolepsy in children and adolescents after vaccination with Pandemrix.
Sarkanen, T. O., Alakuijala, A. P. E., Dauvilliers, Y. A. & Partinen, M. M. Incidence of narcolepsy after H1N1 influenza and vaccinations: systematic review and meta-analysis. Sleep Med. Rev. 38, 177–186 (2018).
Vaarala, O. et al. Antigenic differences between AS03 adjuvanted influenza A (H1N1) pandemic vaccines: implications for Pandemrix-associated narcolepsy risk. PLOS ONE 9, e114361 (2014).
Aran, A. et al. Elevated anti-streptococcal antibodies in patients with recent narcolepsy onset. Sleep 32, 979–983 (2009).
Mahlios, J., De la Herran-Arita, A. K. & Mignot, E. The autoimmune basis of narcolepsy. Curr. Opin. Neurobiol. 23, 767–773 (2013).
Honda, Y. et al. HLA-DR2 and Dw2 in narcolepsy and in other disorders of excessive somnolence without cataplexy. Sleep 9, 133–142 (1986).
Tafti, M. et al. DQB1 locus alone explains most of the risk and protection in narcolepsy with cataplexy in Europe. Sleep 37, 19–25 (2014). This study, drawing upon a large number of subjects, confirms that presence of the DQB1*06:02 allele increases the risk of narcolepsy about 200-fold.
Siebold, C. et al. Crystal structure of HLA-DQ0602 that protects against type 1 diabetes and confers strong susceptibility to narcolepsy. Proc. Natl Acad. Sci. USA 101, 1999–2004 (2004). This study shows that fragments of the orexin peptides fit well within the binding pocket of DQB1*06:02.
Pelin, Z., Guilleminault, C., Risch, N., Grumet, F. C. & Mignot, E. HLA-DQB1*0602 homozygosity increases relative risk for narcolepsy but not disease severity in two ethnic groups. US Modafinil in Narcolepsy Multicenter Study Group. Tissue Antigens 51, 96–100 (1998).
van der Heide, A., Hegeman-Kleinn, I. M., Peeters, E., Lammers, G. J. & Fronczek, R. Immunohistochemical screening for antibodies in recent onset type 1 narcolepsy and after H1N1 vaccination. J. Neuroimmunol. 283, 58–62 (2015).
Miyagawa, T. et al. New susceptibility variants to narcolepsy identified in HLA class II region. Hum. Mol. Genet. 24, 891–898 (2015).
Hor, H. et al. Genome-wide association study identifies new HLA class II haplotypes strongly protective against narcolepsy. Nat. Genet. 42, 786–789 (2010).
Hallmayer, J. et al. Narcolepsy is strongly associated with the T cell receptor alpha locus. Nat. Genet. 41, 708–711 (2009).
Han, F. et al. Genome wide analysis of narcolepsy in China implicates novel immune loci and reveals changes in association prior to versus after the 2009 H1N1 influenza pandemic. PLOS Genet. 9, e1003880 (2013).
Faraco, J. et al. ImmunoChip study implicates antigen presentation to T cells in narcolepsy. PLOS Genet. 9, e1003270 (2013).
Luo, G. et al. Autoimmunity to hypocretin and molecular mimicry to flu antigens in Type 1 narcolepsy. Preprint at https://www.biorxiv.org/content/early/2018/08/24/378109 (2018).
Croft, M., So, T., Duan, W. & Soroosh, P. The significance of OX40 and OX40L to T cell biology and immune disease. Immunol. Rev. 229, 173–191 (2009).
Buckner, J. H. Mechanisms of impaired regulation by CD4+CD25+FOXP3+ regulatory T cells in human autoimmune diseases. Nat. Rev. Immunol. 10, 849–859 (2010).
Mickelsen, L. E. et al. Neurochemical heterogeneity among lateral hypothalamic hypocretin/orexin and melanin-concentrating hormone neurons identified through single-cell gene expression analysis. eNeuro 4, ENEURO.0013-17.2017 (2017).
Azzam, S. et al. Proteomic profiling of the hypothalamus in two mouse models of narcolepsy. Proteomics 17, 1600478 (2017).
Yelin-Bekerman, L. et al. Hypocretin neuron-specific transcriptome profiling identifies the sleep modulator Kcnh4a. eLife 4, e08638 (2015).
Baumann, C. R., Clark, E. L., Pedersen, N. P., Hecht, J. L. & Scammell, T. E. Do enteric neurons make hypocretin? Regul. Pept. 147, 1–3 (2008).
Ahmed, S. S. et al. Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor 2. Sci. Transl Med. 7, 294ra105 (2015).
Bernard-Valnet, R. et al. CD8 T cell-mediated killing of orexinergic neurons induces a narcolepsy-like phenotype in mice. Proc. Natl Acad. Sci. USA 113, 10956–10961 (2016).
Latorre, D. et al. T cells in patients with narcolepsy target self-antigens of hypocretin neurons. Nature 562, 63–68 (2018). This paper identifies a rare T cell population that targets fragments of prepro-orexin.
Kornum, B. R. et al. Absence of autoreactive CD4+ T cells targeting HLA-DQA1*01:02/DQB1*06:02 restricted hypocretin/orexin epitopes in narcolepsy type 1 when detected by EliSpot. J. Neuroimmunol. 309, 7–11 (2017).
Ramberger, M. et al. CD4+ T-cell reactivity to orexin/hypocretin in patients with narcolepsy type 1. Sleep 40, zsw070 (2017).
Lecendreux, M. et al. Narcolepsy type 1 is associated with a systemic increase and activation of regulatory T cells and with a systemic activation of global T cells. PLOS ONE 12, e0169836 (2017).
Tanaka, T., Honda, Y., Inoue, Y. & Honda, M. Detection of autoantibodies against hypocretin, hcrtr1, and hcrtr2 in narcolepsy: anti-hcrt system antibody in narcolepsy. Sleep 29, 633–638 (2006).
Luo, G. et al. Absence of anti-hypocretin receptor 2 autoantibodies in post Pandemrix narcolepsy cases. PLOS ONE 12, e0187305 (2017).
Deloumeau, A. et al. Increased immune complexes of hypocretin autoantibodies in narcolepsy. PLOS ONE 5, e13320 (2010).
Katzav, A. et al. Passive transfer of narcolepsy: anti-TRIB2 autoantibody positive patient IgG causes hypothalamic orexin neuron loss and sleep attacks in mice. J. Autoimmun. 45, 24–30 (2013).
Tanaka, S. et al. Anti-Tribbles pseudokinase 2 (TRIB2)-immunization modulates hypocretin/orexin neuronal functions. Sleep 40, zsw036 (2017).
Bergman, P. et al. Narcolepsy patients have antibodies that stain distinct cell populations in rat brain and influence sleep patterns. Proc. Natl Acad. Sci. USA 111, E3735–E3744 (2014).
Mignot, E. et al. The role of cerebrospinal fluid hypocretin measurement in the diagnosis of narcolepsy and other hypersomnias. Arch. Neurol. 59, 1553–1562 (2002).
Sasai, T., Inoue, Y., Komada, Y., Sugiura, T. & Matsushima, E. Comparison of clinical characteristics among narcolepsy with and without cataplexy and idiopathic hypersomnia without long sleep time, focusing on HLA-DRB1*1501/DQB1*0602 finding. Sleep Med. 10, 961–966 (2009).
Nakamura, M., Kanbayashi, T., Sugiura, T. & Inoue, Y. Relationship between clinical characteristics of narcolepsy and CSF orexin-A levels. J. Sleep Res. 20, 45–49 (2011).
Yin, J. et al. Structure and ligand-binding mechanism of the human OX1 and OX2 orexin receptors. Nat. Struct. Mol. Biol. 23, 293–299 (2016).
US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/show/NCT01789398 (2015).
US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/show/NCT03332784 (2018).
US National Library of Medicine. ClinicalTrials.gov https://clinicaltrials.gov/show/NCT02348593 (2018).
Okun, M. L., Lin, L., Pelin, Z., Hong, S. & Mignot, E. Clinical aspects of narcolepsy–cataplexy across ethnic groups. Sleep 25, 27–35 (2002).
Pizza, F. et al. Clinical and polysomnographic course of childhood narcolepsy with cataplexy. Brain 136, 3787–3795 (2013). This paper provides a detailed description of status cataplecticus and obesity in children with narcolepsy.
Plazzi, G. et al. Complex movement disorders at disease onset in childhood narcolepsy with cataplexy. Brain 134, 3480–3492 (2011).
Willie, J. T. et al. Distinct narcolepsy syndromes in orexin receptor-2 and orexin null mice: molecular genetic dissection of non-REM and REM sleep regulatory processes. Neuron 38, 715–730 (2003).
Bastianini, S., Silvani, A., Berteotti, C., Lo Martire, V. & Zoccoli, G. High-amplitude theta wave bursts during REM sleep and cataplexy in hypocretin-deficient narcoleptic mice. J. Sleep Res. 21, 185–188 (2012).
Hondo, M. et al. Histamine-1 receptor is not required as a downstream effector of orexin-2 receptor in maintenance of basal sleep/wake states. Acta Physiol. 198, 287–294 (2010).
Chemelli, R., Sinton, C. & Yanagisawa, M. Polysomnographic characterization of orexin-2 receptor knockout mice. Sleep 23, A296–A297 (2000).
Hara, J., Yanagisawa, M. & Sakurai, T. Difference in obesity phenotype between orexin-knockout mice and orexin neuron-deficient mice with same genetic background and environmental conditions. Neurosci. Lett. 380, 239–242 (2005).
Lo Martire, V., Silvani, A., Bastianini, S., Berteotti, C. & Zoccoli, G. Effects of ambient temperature on sleep and cardiovascular regulation in mice: the role of hypocretin/orexin neurons. PLOS ONE 7, e47032 (2012).
Kaitin, K. I., Kilduff, T. S. & Dement, W. C. Sleep fragmentation in canine narcolepsy. Sleep 9, 116–119 (1986).
Kaitin, K. I., Kilduff, T. S. & Dement, W. C. Evidence for excessive sleepiness in canine narcoleptics. Electroencephalogr. Clin. Neurophysiol. 64, 447–454 (1986).
Mitler, M. M. & Dement, W. C. Sleep studies on canine narcolepsy: pattern and cycle comparisons between affected and normal dogs. Electroencephalogr. Clin. Neurophysiol. 43, 691–699 (1977).
Lucas, E. A., Foutz, A. S., Dement, W. C. & Mitler, M. M. Sleep cycle organization in narcoleptic and normal dogs. Physiol. Behav. 23, 737–743 (1979).
Ripley, B., Fujiki, N., Okura, M., Mignot, E. & Nishino, S. Hypocretin levels in sporadic and familial cases of canine narcolepsy. Neurobiol. Dis. 8, 525–534 (2001).
Dauvilliers, Y. & Barateau, L. Narcolepsy and other central hypersomnias. Continuum 23, 989–1004 (2017).
Kalogiannis, M. et al. Cholinergic modulation of narcoleptic attacks in double orexin receptor knockout mice. PLOS ONE 6, e18697 (2011).
Kisanuki, Y. et al. Behavioral and polysomnographic characterization of orexin-1 receptor and orexin-2 receptor double knockout mice. Sleep 24, A22 (2001).
Abbas, M. G. et al. Comprehensive behavioral analysis of male Ox1r –/– mice showed implication of orexin receptor-1 in mood, anxiety, and social behavior. Front. Behav. Neurosci. 9, 324 (2015).
Hungs, M. et al. Identification and functional analysis of mutations in the hypocretin (orexin) genes of narcoleptic canines. Genome Res. 11, 531–539 (2001).
Valko, P. O. et al. Increase of histaminergic tuberomammillary neurons in narcolepsy. Ann. Neurol. 74, 794–804 (2013). This paper describes a large increase in histaminergic neurons in the brains of people and mice with narcolepsy.
John, J. et al. Greatly increased numbers of histamine cells in human narcolepsy with cataplexy. Ann. Neurol. 74, 786–793 (2013). This study demonstrates an increase in histaminergic neurons in narcolepsy.
John, J., Wu, M. F., Boehmer, L. N. & Siegel, J. M. Cataplexy-active neurons in the hypothalamus: implications for the role of histamine in sleep and waking behavior. Neuron 42, 619–634 (2004).
Buskova, J., Vaneckova, M., Sonka, K., Seidl, Z. & Nevsimalova, S. Reduced hypothalamic gray matter in narcolepsy with cataplexy. Neuro Endocrinol. Lett. 27, 769–772 (2006).
Kaufmann, C., Schuld, A., Pollmacher, T. & Auer, D. P. Reduced cortical gray matter in narcolepsy: preliminary findings with voxel-based morphometry. Neurology 58, 1852–1855 (2002).
Joo, E. Y., Tae, W. S., Kim, S. T. & Hong, S. B. Gray matter concentration abnormality in brains of narcolepsy patients. Kor. J. Radiol. 10, 552–558 (2009).
Hong, S. B. Neuroimaging of narcolepsy and Kleine–Levin syndrome. Sleep Med. Clin. 12, 359–368 (2017).
The authors acknowledge support from the US National Institutes of Health grants P01 HL095491, R21 NS099787 and R01 NS106032.
Nature Reviews Neuroscience thanks B. Kornum, T. Sakurai and the other anonymous reviewer(s) for their contribution to the peer review of this work.
T.E.S. and C.E.M. made substantial contributions to the discussion of content. All authors wrote the article and reviewed or edited the article before submission.
Correspondence to Thomas E. Scammell.
Vivid, sometimes frightening, dream-like hallucinations that occur when falling asleep (hypnopompic) or immediately after waking (hypnagogic).
An inability to move when falling asleep or immediately after waking.
Muscle weakness or full paralysis triggered by strong, generally positive, emotions.
A disorder characterized by impaired motor inhibition during rapid eye movement sleep, resulting in enactment of dreams.
An abnormally high total amount of sleep over 24 hours.
A prolonged period of moderate to severe weakness with low muscle tone, usually without emotional triggers.
(MHC). A set of immune molecules that bind pathogen-derived antigens and display them on the surface of antigen-presenting cells to promote acquired immune responses.
An allele encoding a human major histocompatibility complex molecule.
A mechanism of autoimmunity in which a foreign antigen is structurally similar to ‘self’-peptides, such that immune cells targeting a pathogen accidentally target healthy tissue.
When the observed frequency of two alleles at two loci occurring together is more frequent than would occur by chance.
The network of sensory and motor neurons that control gut secretions and motility.
(Treg cells). T cells that maintain tolerance to self-antigens by downregulating the activity of effector T cells using anti-inflammatory cytokines and cell-to-cell inhibition.

matches: V. V. V. V. V. V. V. V.


Opinion Judge: SYKES, Circuit Judge.
Party Name: UNITED STATES of America, Plaintiff-Appellee, v. Jeanette GRIGSBY, Defendant-Appellant.
Attorney: Bill Thomas (argued), Attorney, Office of the United States Attorney, Chicago, IL, for Plaintiff-Appellee. Steven Shobat (argued), Attorney, Chicago, IL, for Defendant-Appellant.
Judge Panel: Before BAUER, ROVNER, and SYKES, Circuit Judges.
Bill Thomas (argued), Attorney, Office of the United States Attorney, Chicago, IL, for Plaintiff-Appellee.
Steven Shobat (argued), Attorney, Chicago, IL, for Defendant-Appellant.
Before BAUER, ROVNER, and SYKES, Circuit Judges.
Over the course of seven months, Jeanette Grigsby and several coconspirators planned and executed two bank heists, stealing more than a half-million dollars from the bank where Grigsby worked as a teller. After federal agents uncovered the inside jobs, Grigsby was indicted on two counts of entering a federally insured bank for the purpose of committing a felony. See 18 U.S.C. § 2113(a). She pleaded guilty without a plea agreement to the first count and later stipulated through counsel that she committed the second crime as well. With that, the government moved to dismiss the second count.
the court chose a sentence of 57 months, the top of the range. Grigsby appeals, arguing that the court erroneously applied the two enhancements, and also that her sentence is procedurally defective and substantively unreasonable under 18 U.S.C. § 3553(a).
We affirm. Both enhancements were based on the court's factual finding that Grigsby lied during her plea colloquy in an intentional effort to mislead the court by understating her role in the offense. Although this finding was based largely on documentary evidence— the grand-jury testimony and plea agreements of two of Grigsby's coconspirators— our review remains deferential; we will reverse only for clear error. See 18 U.S.C. § 3742(e). The court's factual finding that Grigsby lied about her role in the offense because she did in fact supervise the scheme is well-supported by the evidence and specific enough to withstand clear-error review. The court also sufficiently considered the § 3553(a) sentencing factors and was not required to specifically address Grigsby's routine arguments for a below-guidelines sentence. Finally, Grigsby's within-guidelines sentence— 57 months for an inside bank-robbery scheme that caused a significant loss— is not unreasonable.
Grigsby was a teller at a branch of Bank One (now Chase Bank) in Oak Forest, Illinois. In the summer of 2005, she and several other employees hatched a plan to steal money from the bank's vault by staging a robbery. On Grigsby's version of events, she reluctantly agreed to participate after repeated prodding from her supervisor Jennifer Barthel, who was an assistant branch manager. According to the other coconspirators, however, it was the other way around; they said it was Grigsby who originated and directed the scheme. Neither Grigsby nor Barthel was a novice at this sort of thing; the women had previously collaborated on a check-cashing scam not at issue in this appeal.
After the plan was conceived, Grigsby approached Tommie Gentry, a recent acquaintance, and asked him to pose as the robber. She gave Gentry the relevant details of the scheme, including a description of the bank's layout and instructions about which teller to approach. She also gave him the code phrase to alert the teller that this was the staged robbery: " Snow White." Grigsby then arranged a couple of meetings with Gentry and Barthel and instructed Gentry to find others to help carry out the robbery. She told Gentry that he and others he recruited would be paid as much as $20,000 apiece from the proceeds. Gentry got his cousin Marcus Gentry to assist.
On the morning of August 24, 2005, the day of the planned robbery, Grigsby and Tommie Gentry met at a nearby McDonald's restaurant to review the instructions. As planned, Grigsby did not participate in the theft itself and called the bank to say that she would not come to work that day. When Tommie and Marcus Gentry arrived at the bank later that morning, they approached the designated teller Miriam Girgis, who was in on the scheme, and she in turn summoned Barthel. Pretending that a robbery was underway, Barthel opened the vault and put a large amount of cash into a black bag that Marcus had carried into the bank. The Gentry cousins then fled the bank and met Grigsby at Tommie's home. Grigsby took possession of the money— totaling about $242,000— and divided it among the coconspirators.
Having been so successful on their first try, Grigsby and her accomplices initiated a second staged robbery about seven months later. Grigsby contacted Tommie Gentry to set things in motion. Gentry, in turn, recruited two new coconspirators.
On March 22, 2006, the day of the second robbery, Grigsby sent Gentry a text message giving him an " all clear" to proceed with the plan. Gentry directed the new recruits to enter the bank. As before, Barthel gave them access to the vault, and they absconded with about $272,500. Grigsby again distributed the money. This time, however, federal agents unraveled the scheme and arrested the culprits.
On August 24th, 2005, I assisted Jenna Barthel, which is my supervisor at the time at Bank One, to stage a bank robbery in which she came to me and asked me that if I knew of anyone that will assist her, she will order the money, she will load the bag up, she will do all of that. I once told her no. Then she asked me again; and then I told her, yeah, but I didn't want to have any parts to do with that; I don't want to be anywhere around. She says, you black; you know that you can get someone to do that; that's what you all do. So I gathered to do such, introduced her to Thomas Gentry. Then he and her proceeded to carry out the act. And doing so, when the— the staged armed robbery had taken place, later on I received monies from that staged bank robbery.
The prosecutor asked a few follow-up questions about whether the bank was federally insured and how much money Grigsby received from the scheme. The district court accepted this as a factual basis for Grigsby's guilty plea. The government moved to dismiss the second count after Grigsby stipulated, through her counsel, that she committed the second offense as well.
Grigsby's presentence report recommended a two-level guidelines enhancement for obstruction of justice, see U.S.S.G. § 3C1.1, based on her sworn statement to the court at her guilty-plea hearing in which she substantially understated her role in the offense. The presentence report also recommended a three-level enhancement under U.S.S.G. § 3B1.1(b) for Grigsby's supervisory role in the scheme. At sentencing the prosecutor submitted Barthel's and Tommie Gentry's grand-jury testimony and written plea agreements to prove that Grigsby in fact supervised the scheme and lied about her role during her plea colloquy. Notwithstanding its position on the obstruction-of-justice enhancement, the government did not object to a three-level reduction for acceptance of responsibility, see id. § 3E1.1(b), based on Grigsby's timely guilty plea and her stipulation to the second robbery.
I agree with the government. There was an obstruction of justice here. There was a clear material— let me make it clear— a clear material misrepresentation as to what her role in the offense was. She turned it upside down. Everything she said was contradicted by the others with respect to what her role was, and that was for the purpose of escaping culpability.
I think there are several witnesses or multiple witnesses who make this defendant clearly a recruiter and a decision-maker and an organizer. First, her coworkers say she recruited them, not the other way around. Tomm[ie] Gentry says clearly she recruited him. No one else recruited him. No one else reached out to him. She did. And recruiting co-conspirators is one of the things one looks at in determining whether an adjustment for role in the offense is appropriate.


§ 257-41 Meters required; charge.
§ 257-42 Furnishing of meters; ownership; charges.
§ 257-43 Replacement of meters.
§ 257-44 Location of meters.
§ 257-45 Maintenance of meters.
§ 257-46 Testing of meter at owner's request.
§ 257-47 Fixing of charges when meter is inaccurate.
§ 257-48 Number of meters.
§ 257-49 Removal or interference with meter; penalty.
§ 257-50 Meter glasses; maintenance of glasses, dials and spindles.
§ 257-51 Premises where water may be obtained for more than one service.
Water shall be obtained from the mains of the water distribution system only through a metered service, with the exception of temporary usage during authorized building construction or temporary use, as set forth in § 257-11 upon arrangement with the Board of Trustees. When meters are furnished for temporary service, a fee, as set forth in the fee schedule, of the Village of Brewster, will be required by the Village Board of Trustees for each meter.
Meters will be furnished by and remain the property of the Village. The actual meter cost and installation shall be the responsibility of the owner. In the event a request is made by an owner to move a meter, there shall be a charge, as set forth in the fee schedule, for the removal and reinstallation of the meter, even in the event the reinstalled meter is an upgraded model.
Three-quarter-inch meter: charge as set forth in the fee schedule.
One-inch meter: charge as set forth in the fee schedule.
One-and-one-half-inch meter: charge as set forth in the fee schedule.
Two-inch meter: charge as set forth in the fee schedule.
This meter charge will be reflected on the quarterly water bill.
Meters shall be located in the building and must be installed by a licensed contractor acting as agent for the owner, under the supervision of the Superintendent or his authorized representative thereof, in a horizontal position, not more than three feet from the point where the service enters the building. A suitable valve shall be installed on the inlet and outlet side of the meter and a double check valve, Watts or equivalent, as approved by the Superintendent and/or the Village Engineer, on the outlet side of the meter where necessary. Attention of the property owner is called to the fact that in some instances it will be necessary to install relief valves on the plumbing system on the inlet side of the meter within the building. The meter must be kept accessible at all times. The employees and agents of the Village may enter the premises of the owner at any reasonable time to examine the pipes and fixtures, the quantity of water used and the manner of its use. For the purpose of this article, the hours from 8:00 a.m. to 6:00 p.m. shall be considered reasonable.
Meters shall be read periodically by the Superintendent or his designee. When this is not possible, the Superintendent will leave a notice to gain access and the owner must comply within two weeks.
The Village shall have no liability for any damage caused to any property due to any malfunction or damage to the meter. All such damage shall be the responsibility of the owner. Should a meter become frozen or otherwise damaged, it shall be repaired by the Village at the expense of the owner. The minimum charge for such repair shall be set forth in the fee schedule of the Village of Brewster.
If the meter is not registering properly, the owner may file a complaint with the Village, whereupon the meter will be removed and tested by the Superintendent or his designee. If it is found to register against the owner by more than 2%, there will be no charge for removing, repairing and resetting the meter. If, however, the meter is not found to register against the owner by more than 2%, a minimum charge, as set forth in the fee schedule, will be made for the test.
Should the meter not register properly, the Board of Trustees may, at its option, fix the charge against the owner by the average consumption rate according to the consumption during a previously corresponding period.
No more than one meter shall be furnished for each service line. Any exceptions or requests for additional meters must be approved by the Board of Trustees.
All persons are hereby forbidden to interfere with or remove a water meter from any service after it has been attached, under a penalty of $100 plus the actual cost of replacement for each offense, in addition to any and all penalties under § 257-88 of this chapter.
Dirty meter glasses and dials will be cleaned and leaky spindles packed by the Superintendent, without charge.
In any premises where water may be obtained through more than one metered service, the Village reserves the right to shut off and seal any service.
No seal placed by the Village for the protection of any meter, valve, fitting or other water connection shall be tampered with or defaced. It shall not be broken except on written authorization from the Village. Where the seal is broken, the Village reserves the right to order the meter removed for testing at the expense of the owner and upon a penalty of $50, in addition to any and all penalties under § 257-88 of this chapter.


text:
The CJEU Grand Chamber, with judgment of 6 October 2015 (Delvigne case), ruled out that French law depriving some individuals convicted by means of a final judgment of their right to vote was incompatible with a number of principles of the EU Charter of Fundamental Rights (Articles 39 and 49). The judgment was already commented in this blog by Marco Borraccetti.
The decision is important because it is the first time that the CJEU has issued judgment in this specific type of matter (for the CJEU’s case-law on the right to vote to the European Parliament’s elections see Borraccetti) whereas the ECtHR has ruled many times in similar cases in connection with the application of Article 3 of Protocol No. 1 to the Convention (right to free elections), in particular against the United Kingdom (e.g. GC, Hirst v. UK (No. 2) , 6 October 2005; Greens and M.T. v. UK, 23 November 2010; Firth and Others v. UK, 12 August 2014) and other ECHR Contracting States (e.g. Frodl v. Austria, 8 April 2010; GC, Scoppola v. Italy (No.3), 22 May 2012; Söyler v. Turkey, 17 September 2013; Murat Vural v. Turkey, 21 October 2014; and Anchugov and Gladkov v. Russia, 4 July 2013). The importance of the ECtHR’s case law has been defined as “the prisoner voting saga” (Milanovic).
The relevance of the CJEU’s judgment was immediately highlighted in the English press (e.g., the Guardian), which called the decision an «unexpected ‘ruling’» which «has clear implications for Britain’s blanket ban on prisoner voting».
The CJEU’s ruling arose out of a request for a preliminary ruling from the Tribunal d’instance de Bordeaux in the context of proceedings involving Mr. Delvigne on the one part and the Municipality of Lesparre-Médoc and the Prefect of Gironde on the other part.
Delvigne was convicted in France of a serious crime and given a custodial sentence of 12 years by a final judgment delivered in 1988. By operation of law that conviction automatically entailed the loss of Mr Delvigne’s civic rights, including deprivation of his right to vote. A French law of 1992 then abolished the de jure loss of civic rights for persons whose conviction was final, providing that the total or partial deprivation of one’s civic rights had to be decided by a court and in any event could not exceed ten years (maximum sentence for conviction of a serious offence). However, the new law maintained the loss of civic rights (and hence the right to vote) for those whose conviction had become final before the entry into force of the more lenient rule, which covered Mr. Delvigne’s situation, affording those individuals the option of applying to the court to obtain the lifting of the said additional penalty.
The questions put to the CJEU essentially concerned whether the French law applied to Delvigne was compatible with the EU Charter of Fundamental Rights, specifically Article 39 (right to vote and to stand as a candidate at elections to the European Parliament), with reference to the deprivation of his right to vote in European Parliament elections, and Article 49 (principles of legality and proportionality of criminal offences and penalties), with reference to the failure to comply with the provision to the effect that “if subsequent to the commission of a criminal offence, the law provides for a lighter penalty, that penalty shall be applicable”.
The CJEU ruled out any violation of those principles enshrined in the EU Charter.
As regards Article 39, the Court asserted that the deprivation of the right to vote is «provided for by law» and «respects the essence» of this right because it «does not call into question that right as such, since it has the effect of excluding certain persons, under specific conditions and on account of their conduct, from those entitled to vote in elections to the [EU] Parliament». The CJEU added that the said limitation does not conflict with the principle of proportionality since it «takes into account the nature and gravity of the criminal offence committed and the duration of the penalty» (paras. 47-49 of the Judgment). On that point, it is worth remembering that those conditions for lawfulness of domestic legislation limiting the right to vote of detainees had been laid down in ECtHR case-law.
As regards Article 49, the Court fully endorsed the arguments of the French Government and only stated that the principle of the retroactive effect of a more lenient criminal law was not breached in the present case since the legislation in question «is limited to maintaining the deprivation of the right to vote resulting, by operation of law, from a criminal conviction only in respect of final convictions by judgment delivered at last instance under the old Criminal Code» (para. 56 of the Judgment).
Finally, with reference to the issue of the proportionality of the French law in relation to the application of the EU Charter, the Court considered as decisive the fact that a person in Mr Delvigne’s situation could apply to the relevant court to lift the additional penalty of loss of civic rights.
In our view the CJEU’s judgment suffers from a number of evident shortcomings in terms of both the method used to reach the decision in question and some substantive aspects.
From a methodological standpoint, two criticism come to mind. The first concerns the total absence of any reference to the domestic legislation of the other EU Member States for the specific purpose of understanding whether, in light of the limitations on Mr. Delvigne right to vote, ‘the essence’ of that right and above all the principle of proportionality were respected. In this regard a comparison between the CJEU’s judgment and the ECtHR’s case-law is frankly embarrassing if one considers that the ECtHR conducted an in-depth survey of the domestic legislation of the Contracting States of the ECHR (legislation that is suitably classified by the ECtHR on the basis of whether it maintains or restricts in whole or in part the right to vote of detainees) and even analysed the relevant case-law from non-European States (Hirst (No. 2), paras. 33-39). This ECtHR approach is used to check that Contracting States have not adopted legislation that goes beyond their margin of appreciation (ever smaller under ECtHR case law).
The second criticism regarding methodology consists of the apparently inexplicable fact (although in reality the explanation is simple and lies in a clumsy attempt to conceal a clear contrast with the ECtHR’s case-law) that the CJEU makes no reference at all to the abundant case-law of the ECtHR. This notwithstanding that the Preamble of the EU Charter reaffirms the rights as they result inter alia from the ECHR and the case-law of the Court of Justice of the European Communities [Union] and the ECtHR and that Article 52 (3) of the Charter states that «in so far as this Charter contains rights which correspond to rights guaranteed by the Convention for the Protection of Human Rights and Fundamental Freedoms, the meaning and scope of those rights shall be the same as those laid down by the said Convention». This choice is even more questionable because the conditions laid down by the CJEU to check the lawfulness of national measures that limit the right to vote of detainees are, as mentioned above, drawn precisely from ECtHR case-law.
Turning now to substance, first and foremost one can criticise the assertion that there is no violation of the rights of detainees who are in the same particular position as Delvigne because they can always apply to a court to lift the ban and hence have their right to vote restored. With due respect to the CJEU, relying on a court’s discretion (even if bound by the provisions of law) is completely different from enjoying a right expressly provided for by law upon lapse of the additional penalty due the expiry of the period of time envisaged by the new domestic law on impediments to voting rights. The difference between the two situations is plain if one considers that the ECtHR, examining the laws of the Contracting States of the ECHR, stated that in France «prisoners may vote if the right is given by the court» (Hirst (No. 2), para 33, footnote 2). Moreover, in cases like Delvigne, judicial intervention is even not certain since it occurs at the request of the party concerned and thus it contradicts one of the conditions laid down by the ECtHR according to which «it is an essential element that the decision on disenfranchisement should be taken by a judge, taking into account the particular circumstances» of the case (Frodl, para. 34).
Moreover, as regards the substance of the judgment, it is necessary to dwell on the application of the principle of proportionality, which in the present case plays a fundamental role. It is our view that in the circumstances the CJEU should have considered as disproportionate the national law that maintains a voting ban for those whose conviction had become final (before the entry into force of the new law). This is because the law is entirely unreasonable and discriminatory if one considers that for the same cases occurring after the entry into force the law provides for a more lenient additional penalty. Furthermore, one cannot rule out that the domestic law in question could even be held to be such as to jeopardise the very essence of the right to vote of detainees who find themselves in that same specific position since they are potentially deprived of their voting rights indefinitely.
The CJEU’s judgement on the right to vote for prisoners as self-contained case-law?
As mentioned the CJEU made no reference to either the domestic law of the EU Member States or the case-law of the ECtHR. It would therefore seem to be an expression in this subject of a self-contained regime or better still a self-contained case-law.
In our view, the rationale for that (well thought out) choice made by the CJEU resides in a will to not openly reveal the evident contrast between the case-law of the ECtHR and the CJEU. It is in fact indisputable that the margin of appreciation afforded by the ECHR to the Contracting States has been gradually reduced as regards precluding the voting rights of detainees, in terms of both the application of pre-existing domestic law and the specific changes thereto (due to a need to comply with the ECHR), bearing in mind moreover that at times the preclusion of voting rights applies to individuals on conditional release and even to those who are given suspended sentences and therefore do not even serve a prison term (Söyler, para. 38). This is clear if one analyses the ECtHR’s case-law concerning the United Kingdom and the adoption, under Article 46 of the ECHR, of the pilot judgment procedure, with an express indication that, in the case of the UK «the only relevant remedy is a change in the law», setting a short timetable for the adoption of that legislation, i.e. six months after the date the Greens and M.T. judgment became final (paras. 118 and 115).
In light of the above, we believe that a case similar to Delvigne (or indeed that same case should the applicant decide to pursue legal action and pass the admissibility test envisaged by the ECHR) would have a different outcome before the ECtHR. In this regard the central point (but not the only one) of the question lies in the failure to apply the more lenient penalty introduced by a subsequent law. This circumstance could be criticised by the ECtHR, in terms of disproportionality of the national measures, when establishing a breach of Article 3 of Protocol No. 1, and in terms of violating the principle contained in Article 7 of the ECHR (no punishment without law, which includes the application of the lex mitior to individuals convicted by means of a final judgment). Naturally, the ECtHR could well find that both provisions of the Convention have been breached.
It therefore seems to us that the saga of detainees has not ended yet and, on the contrary, this new chapter could give rise to a further instance of contrasting case-law between the CJEU and the ECtHR. We remain seized on the matter!
Verso una maggiore effettività del legal aid in Europa?

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WILLIAM H. PAULEY III, District Judge.
Plaintiff pro se Seth Mitchell seeks judicial review under 42 U.S.C. § 405(g) of a final decision of the Commissioner of Social Security (“Commissioner”) denying his application for supplemental social security income. On November 7, 2016, this Court referred the matter to the assigned Magistrate Judge for a Report & Recommendation. Prior to the referral, Mitchell moved for summary judgment. On March 20, 2017, the Commissioner cross-moved for judgment on the pleadings. On February 2, 2018, Magistrate Judge Pitman issued a Report & Recommendation (the “Report”), recommending that this Court deny Mitchell's motion and grant the Commissioner's cross-motion. Mitchell filed objections to the Report. This Court reviewed Mitchell's objections, concludes that they lack merit, and adopts Magistrate Judge Pitman's thorough and well-reasoned Report.
A district court “may accept, reject, or modify, in whole or in part, the findings or recommendations” of a magistrate judge. 28 U.S.C. § 636(b)(1). This Court reviews de novo the portions of the Report to which objections are made and reviews the remainder for clear error on the face of the record. 28 U.S.C. § 636(b)(1); Mulosmanaj v. Colvin, 2016 WL 4775613, at *2 (S.D.N.Y. Sept. 14, 2016). In order to warrant de novo review, the objections “must be specific and clearly aimed at particular findings in the magistrate judge's proposal.” George v. Prof'l Disposables Int'l, Inc., 221 F.Supp.3d 428, 433 (S.D.N.Y. 2016) (citation and quotation mark omitted). Objections that are conclusory or general are entitled to only clear error review. Pineda v. Masonry Const., Inc., 831 F.Supp.2d 666, 671 (S.D.N.Y. 2011).
A Commissioner's determination regarding a claimant's disability may only be set aside “if the factual findings are not supported by ‘substantial evidence' or if the decision is based on legal error.” Shaw v. Carter, 221 F.3d 126, 131 (2d Cir. 2000). Substantial evidence is “more than a mere scintilla. It means such relevant evidence as a reasonable mind might accept as adequate to support a conclusion.” Richardson v. Perales, 402 U.S. 389, 401 (1971).
Mitchell first contends that the Report incorrectly characterizes a finding by Dr. Goldman, a psychologist who rendered a consultative psychiatric evaluation, by stating that Dr. Goldman “ruled out a diagnosis of PTSD.” (Report, ECF No. 67, at 19, 53.) On review of the psychiatric evaluation, this Court concludes that the relevant language in Dr. Goldman's report is ambiguous. (See SSA Administrative Record, ECF No. 20 (“Record”), at 323-26.) Specifically, after detailing Mitchell's symptoms of anxiety, Dr. Goldman stated “Rule out posttraumatic stress disorder” in a section labeled as “DIAGNOSIS.” (Record at 326.) Mitchell contends that because Dr. Goldman recommended “[p]sychiatric intervention, ” the only possible reading is that she meant to recommend a psychiatric intervention only to rule out PTSD. But it is equally reasonable that Dr. Goldman recommended psychiatric intervention to address Mitchell's anxiety-related issues in light of her evaluation of his prognosis as “[f]air given that he receive psychiatric intervention”-a prognosis that makes little sense if the psychiatric intervention were only for the purposes of ruling out PTSD. (Record at 326.) Given this ambiguity, this Court sees no error in Magistrate Judge Pitman's characterization and declines to modify or reject it.
Next, Mitchell argues that ALJ Thomas Grabeel violated the “treating physician rule” by assigning minimal weight to Dr. Goldman's opinion. Under the “treating physician rule, ” the ALJ must “give ‘controlling weight' to a treating physician's opinion as to the nature and severity of a claimant's impairments, as long as it is ‘well-supported by medically acceptable clinical and laboratory diagnostic techniques and is not inconsistent with other substantial evidence in [the] case record.'” Lebron v. Colvin, 2015 WL 1223868, at *10 (S.D.N.Y. Mar. 16, 2015) (citing 20 C.F.R. § 416.927(c)(2)). This objection is meritless, however, because Dr. Goldman was not a treating physician, but a consultative psychologist who conducted a one-time examination of Mitchell. See Rogers v. Astrue, 895 F.Supp.2d 541, 550 (S.D.N.Y. 2012) (explaining that the “treating physician rule” should not be applied where the examiner was not the claimant's treating physician during the relevant time period).
Mitchell also objects to Magistrate Judge Pitman's statement and application of the legal standard for determining whether the claimant has a disability. Specifically, he contends that the “plausibility standard” applies-i.e., making the disability determination based on a court's “judicial experience and common sense.” As an initial matter, this contention does nothing more than reiterate the same argument he made to Magistrate Judge Pitman. (ECF No. 49, at 4.) See Ortiz v. Barkley, 558 F.Supp.2d 444, 451 (S.D.N.Y. 2008) (“It is improper for an objecting party to attempt to relitigate the entire content of the hearing before the Magistrate Judge by submitting papers to a district court which are nothing more than a rehashing of the same arguments and positions taken in the original papers submitted to the Magistrate Judge.” (quotation marks omitted)). Moreover, the standard that Mitchell maintains should be applied has no applicability here. See Viti v. Guardian Life Ins. Co. of Am., 817 F.Supp.2d 214, 223 (S.D.N.Y. 2011) (stating the standard on a Rule 12(b)(6) motion to dismiss). Both Magistrate Judge Pitman and ALJ Grabeel applied and analyzed the five-step analysis required by 20 C.F.R. § 416.920 to determine whether Mitchell was disabled.
Separately, Mitchell appends two exhibits to his filed objections. The first is a reasonable accommodation inquiry submitted in connection with Mitchell's employment at Macy's, and the second is a federal complaint that Mitchell filed against Goldman Sachs that purports to fill gaps in the administrative record.


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I.e., two courtyards with two houses opening into each. V. 'Er. 5a and 73b.
And for this reason when the courtyards are combined with the houses it is not permissible to carry save within four cubits.
The tenants of all the houses save one can renounce their rights in the courtyard in his favour; the courtyard is then his, and he may carry from his house into it.
Whereas Rab needs at least two houses, v. p, 654, n. 8.
Rab holds ('Er. 74a) that a roof, courtyards, enclosures, and the alley are all one domain, and carrying is permitted from one to another, provided, however, that the houses are not combined with the courtyards, so that no utensils belonging to the houses are to be found in the courtyards which might then be carried into the alley. Hence the same applies to carrying in the alley itself: for if there are no houses at all a formal partnership is unnecessary, and carrying in the alley is permitted, just as from the alley into the courtyard. Since the houses are not combined with the courtyards and no utensils may be moved from the former into the latter, for all practical purposes the houses are non-existent: therefore one may carry over the whole of the alley itself.
As distinct from the precept itself.
Which are offered on the Feast of Weeks, v. Lev. XXIII, 17.
Sc. the Feast of Weeks, and must not be postponed for the next day.
That their baking supersedes the Sabbath; not the baking, but the offering 'unto the Lord' is the actual precept, the former being merely a necessary preparation.
V. Glos. But if he held that all preparations supersede the Sabbath, the would not require the gezerah shawah in this particular case.
Viz., the reaping, grinding. and sifting; Men. 72a.
I.e., from the day that ye brought (v. 15) and 'ye shall bring' (v. 17) must have no other purpose than this gezerah shawah. There are three views on this matter: (i) Both parts of the gezerah shawah must be free, otherwise it can be refuted if they are dissimilar in other respects; (ii) Only one part must be free; and (iii) Even if both parts are required for another teaching too, the gezerah shawah cannot be refuted.
But not for the express purpose of fulfilling the precept.
Since Scripture could write, and ye shall offer a new meal-offering unto the Lord out of your habitations etc. The extension embraces the preliminaries of bringing, and intimates that these supersede the Sabbath.
R. Johanan's statement that R. Eliezer did not rule that the preliminaries of all precepts etc.
V. Glos. and Lev. XXIII, 40.
V. Glos. and ibid. v. 42.
V. Glos. and ibid. v. 24.
These must not be inserted or affixed on the Sabbath.
'The sukkah and all its preliminaries supersede the Sabbath: this is R. Eliezer's view.' Whence does R. Eliezer learn this? If from the 'omer and the two loaves, — [there it may be] because they are requirements of the Most High; if from lulab, — [that may be] because it requires four species! Rather [the scope of] seven days' is deduced from the 'seven days' of lulab: just as there its preliminaries supersede the Sabbath, so here too its preliminaries supersede the Sabbath.19 Then let the Divine Law write it in connection with sukkah, and these [others] could be adduced and learnt therefrom? — Because one could refute [the analogy]: as for sukkah, that is because it [the precept] is binding by night just as by day.
Thus, when he comes to do it on the Sabbath, he could renounce ownership of the garment or the house, in which case these precepts are no longer incumbent on him.
I.e., they are a direct offering.
For 'on the first' suffices: hence 'day' teaches that the ceremony must be performed whatever the day.
Permitting the handling of the lulab on the Sabbath.
Surely not, for the interdict of handling is only Rabbinical.
E.g., carrying the lulab through the streets, which would otherwise be Biblically forbidden.
How do they interpret the superfluous 'day'?
The lulab precept has to be performed by day.
Do they not admit that it can be deduced from this latter verse?
This is deduced in Suk. 43a.
This law that the preliminaries supersede the Sabbath.
Sc. the 'omer and the two loaves.
That there too it is thus: why are separate verses required?
Vis., those enumerated in Lev. XXIII, 40. Hence it is important that even its preliminaries supersede the Sabbath.
Since this analogy is based on a gezerah shawah, it cannot be refuted as before, when the suggested analogy was based purely on logical grounds. (Rashi).
Lev. XXIII, vv. 6 and 39.
They too must partake thereof; v. Pes. 43b. But the precepts of lulab and sukkah are not incumbent upon women.
Does 'day' extend the law even to the Sabbath.
This is rather unusual. Generally we have 'the School of R. Ishmael', and the present passage is so quoted supra 117b in cur. edd. R. Han. however, reads 'the School of Samuel' there too, and it is likewise so in R.H. 29b in cur. edd. Weiss, Dor, III, p. 169 maintains that the reference is to a collection of Baraithas compiled by Samuel. It may also be observed that the verse quoted here is not the same as that quoted supra in cur. edd., though Tosaf.'s reading is identical in both places. It is barely possible that two different Baraithas are referred to, both making the same deduction but from different verses.
Hence no verse is required to teach that it is permitted.
Sc. the blowing of the shofar on New Year and on the day of atonement.
As shown in R.H. 33b.
Hence it is so important that even its preliminaries supersede the Sabbath. But the same may not apply to other precepts.
In accordance with Lev. XXV, 10. Hence this too was of particularly great importance.
Each differs in some respect.

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On January 23, 2015, the Department Of Veterans Affairs issued proposed regulations which would make significant changes to the determination of Net Worth, the treatment of pre-application Asset Transfers, and the deductibility of medical expenses in determining countable income.  To the extent these become final, they will dramatically impact planning strategies that advocates have long used to help veterans and their surviving spouses qualify for pension. Likewise, they will also impact both Medi-Cal planning and potentially even garden-variety estate planning.
Veterans advocates question whether the proposed regulations are grounded in statutory authority and court challenges on that basis are anticipated.  Pending those challenges, this article raises alerts for advocates considering asset transfers to help veterans qualify for pension.
It appears that the primary purpose of the proposed regulations was to “reduce opportunities for attorneys and financial advisors to take advantage of pension claimants” by recommending asset transfers and the restructuring of assets in order to qualify for pension. While ostensibly designed to prevent this perceived overreach by advisors, the regulations would instead severely punish deserving veterans and their dependents.
In its proposed regulations, the VA proposes harsh new rules to penalize asset transfers made within 36 months of application. This proposal represents a sea-change for the VA. Historically, asset transfers made prior to application were perfectly fine, providing that the transfers were made to a person who was not a part of the veteran’s household, and where the veteran maintained no ownership, dominion or control of the transferred assets.
By contrast, the proposed regulations would now create a presumption, absent clear and convincing evidence showing otherwise, that uncompensated asset transfers made during the 36 month pre-application “look back” period prior to application were made to establish pension entitlement. The VA would establish a penalty period of up to 10 years for claimants who transferred assets for less than fair market value to qualify. The penalty period would be calculated based on the uncompensated value of assets transferred during the look back period to the extent the transferred assets would have otherwise caused the Veteran’s Net Worth to exceed the applicable Net Worth ceiling. These “excess assets” are called “covered assets” in the proposed regulations. Exception: assets transferred to a trust created exclusively for a disabled child of the veteran, whose disability began before age 18, are not treated as covered assets and would not trigger a penalty period. 38 CFR § 3.276(d).
The penalty for the transfer of covered assets would be determined as follows: the value of covered assets transferred during the look back period would be divided by the applicable monthly pension rate for Aid and Attendance at the time of the VA pension claim, and then rounded down to the nearest whole number. That number would then be the number of months of disqualification. 38 CFR §3.276(e).
In essence, the duration of the penalty would depend upon the marital status of the claimant and the applicable monthly Aid and Attendance rate at the time of application. 38 CFR § 3.276(e)(1). In this regard, note that the transfer penalty for a surviving spouse would be approximately double what it would be for a married veteran.
On the good side  , the regulations propose a “bright line” test for determining Net Worth by anchoring the determination to the Medicaid rules. Under the proposed regulations, Net Worth would be the sum of the following: (1) the maximum Community Spouse Resource Allowance (currently, $119,220 for 2015), annually indexed for inflation, plus (2) the amount of the Veteran’s annual household income. It appears that this “bright line” would apply both to a single veteran as well as to a married veteran. On its face, this use of the maximum CSRA as the “bright line” Net Worth ceiling would bring more predictability to adjudications of Net Worth. However, adding annual income to the tally of Net Worth would effectively reduce the CSRA “bright line” ceiling.
The other bit of qualified good news is the proposed treatment of the home. In current practice, and notwithstanding the absence of statutory or regulatory authority, advocates report that some VA adjudicators include the home in Net Worth if the veteran has moved out of the home to a care facility and rents out his home. Under the proposed rules, the home – up to a 2 acre lot area –would not be counted as an asset even if the claimant resides outside the home in order to receive care. 3.275(b)(ii). By inference, a gift transfer of the home would presumably not trigger a transfer penalty as it would not be deemed an asset for Net Worth purposes, although the regulations do not expressly so state. However, if the home were sold, the proceeds would be treated as an asset, except to the extent they are “used to purchase another residence within the same calendar year”. 38 CFR §3.275(b)(1) [emphasis added]. As proposed, end of year sales would pose a problem, as there would not likely be enough time to purchase a replacement home to exempt the proceeds.
Heretofore, when advocates considered asset transfers for a veteran faced with long-term care, the focus had been entirely upon the Medi-Cal rules, rather than upon the VA pension rules. Reason: Asset transfers under the Medi-Cal program triggered penalty periods, while asset transfers under the VA Pension program did not. Thus, asset transfers made in compliance with the Medi-Cal program were necessarily compliant with the VA pension program.
Now, under the proposed regulations, that approach would be turned on its head: both programs would penalize asset transfers, but the potential period of disqualification under the VA pension program would be much longer. Reason: the penalty divisor under VA program would be much smaller than the Medi-Cal penalty divisor, resulting in a longer period of disqualification for VA Pension claimants. Further, the penalty could extend up to 10 years under the VA program, while it is currently capped at 30 months under the Medi-Cal program.
Thus, under the proposed new regulations, Veterans who opt for Medi-Cal planning may need to forego application for a VA Pension, at least during the 36 month look-back period.
2) The Effective Date of the Proposed Regulations Is Unknown: Retroactive?
The regulations do not set a date as to when they would become effective. Could they be retroactive to some date earlier than the date of the Final Regulations? Advocates should, even now, be wary of advising asset transfers to qualify for VA pension until that effective date is known.
There is no provision in the proposed regulations to grandfather existing claims, and – – absent clarity on that point — there is some concern that claimants who currently receive pension, and who previously participated in pre-application asset transfers in compliance with then existing rules, could have their claims re-determined under the proposed new rules. Further, there is no “phase-in” with regard to pre-application asset transfers as there likely will be for Medi-Cal eligibility when the Deficit Reduction Act is implemented in California.
4) The Purchase of an Annuity Would Be Considered an Uncompensated Transfer.
The proposed regulations do not recognize that a lump-sum single premium used to purchase an annuity is a purchase for value, i.e. a lump sum payment in exchange for a stream of payments. Instead, they treat the entire premium as an uncompensated transfer. 38 CFR § 3.276(a)(6). This treatment would seem to eliminate the use of annuities as a means to reduce excess assets to meet Net Worth limitations, at least if purchased within the “look-back” period. Further, to the extent that the purchase of an annuity might be considered appropriate for Medi-Cal planning, it would have potentially adverse implications for a client also considering application for VA pension.
5) Transfers to Any Trust Would Be Deemed an Uncompensated Transfer: Estate Planning Implications.
Except as noted below, the proposed regulations treat the transfer to any trust as an uncompensated transfer. 38 CFR § 3.276(a)(6). This is especially problematic as they do not distinguish between an irrevocable trust, on the one hand, and a revocable trust, on the other. This failure to distinguish one trust from the other is, again, a trap for the unwary. As presently formulated, a veteran who creates and funds a garden-variety Living Trust within 36 months of application could run afoul of the transfer provisions.
Exception: transfers to a trust set up for exclusively for a disabled child of the veteran, provided the child’s disability began before age 18. 38 CFR § 3.276(d).
For purposes of calculating the penalty, the proposed regulations appear to aggregate all uncompensated transfers made within the 36 month pre-application look-back period. Further, they provide that if the claimant made more than one transfer during that period, the penalty would not begin to run until the 1st day of the month following the date of the last transfer. 38 CFR § 3.276(e)(2). This treatment creates a longer period of disqualification and differs from the way Medi-Cal currently treats asset transfers (i.e., as running from the date of each individual transfer).
The current regulations require that all of the covered assets must be returned in order to avoid the position of a penalty. 38 CFR § 3.276(e)(5). Notably, there is no provision for a reduction in penalty based upon a partial return of assets. Thus, if the gift recipient has spent some or all of the gifted assets and cannot return 100% of them to the veteran, the veteran will incur a full penalty period.
8) Narrow Window to Reverse Gift Transfers; Trap for the Unwary.
A transfer penalty could only be avoided if all of the transferred assets were returned back to the claimant before filing the claim or within 30 days of filing and evidence of such return is provided to the VA within 60  days of the VA’s advice of its intention to impose a penalty. This 30 day window is a trap for the unwary: the veteran may have long since forgotten about the transfer and/or may not know that it is subject to a penalty calculation until he is later so advised and it is then long past the 30 day cure window. Further, if the effective date of the regulations is anchored to the time of application without grand-fathering prior transfers, veterans who made lawful, uncompensated transfers under prior law would be heavily penalized when they later apply for pension.
While the proposed VA regulations are, in part, anchored to the Medicaid rules, many accepted Medicaid strategies will not work to qualify for pension. Example: Medicaid applicants in states already operating under the Deficit Reduction Act (“DRA”) sometimes bridge the penalty period by purchasing a DRA compliant annuity or arranging an intra-family installment loan to cover care expenses during the penalty period. This DRA bridging technique is unlikely to work in the context of pension: the purchase of an annuity to reduce Net Worth, in and of itself, would be treated as a prohibited transfer, and the installment note would likely be valued as an asset in the calculation of Net Worth.
This limited exception exposes the harsh penalty calculation to even innocent transfers made for a purpose other than to qualify for pension, e.g. to help with wedding expenses, college education, and the like.
The application of the penalty calculations can lead to skewed results, in this sense: if the transfers were made while the veteran was married, the penalty divisor would be $2,120 (Aid and Attendance for a married veteran in 2015), but if the veteran later dies and application for pension is made by his surviving spouse, the penalty divisor would only be $1,149 (Aid and Attendance for a Surviving Spouse in 2015). The smaller the divisor, the longer the penalty period. Advocates question whether this disparate treatment makes sense, even in the context of the avowed purpose of discouraging uncompensated transfers during the look-back period.
Even now, because of the lack of clarity regarding the effective date of the proposed changes, advocates should be extremely cautious about continuing to advocate the use divestment strategies to help claimants qualify for VA pension. Further, where veterans have already made uncompensated transfers within the prior 36 months, advocates should consider advising them to defer application for pension to a date more than 36 months after the last such transfer. They should also advise that divestment strategies used for Medi-Cal planning may adversely impact eligibility for pension. Likewise, the purchase of annuities should no longer be viewed as a tool to reduce Net Worth. Further, veterans and/or their spouses who choose to create “Living Trusts” should be advised of the potential implications of these devices should they seek a VA pension within 36 months of funding.
Even under the proposed regulations, there is still a place for VA pension planning. However, to the extent that planning is focused upon reducing Net Worth, it will now become a more proactive undertaking in that it will need to be completed more than 36 months before application.
. Federal Register, Volume 80, Number 15, Part IV. The amendments propose to amend 38 CFR §’s 3.261 — 3.551.
. Two prior reform bills in Congress died in committee. The VA’s proposed regulations, while prompted by recommendations made by the Government Accountability Office (GAO, ignore the GAO’s own specific recommendation that the VA obtain clear statutory authority from Congress to establish “a look back and penalty period” similar to other means tested programs. GAO, “Report to Congressional Requesters; VETERANS PENSION BENEFITS: Improvements Needed to Ensure Only Qualified Veterans and Survivors Receive Benefits”, at page 22. Advocates also argue that the proposed regulations are “arbitrary and capricious”.
 Some advocates feel that the proposed CSRA Net Worth cap, reduced by annual income, is unduly limiting, especially for veterans with significant ongoing care expenses that will require they consume all of their savings before end of life.
. There seems to be an error in the proposed regulations. The explanatory comment preceding the regulations refers to a 90 day period (at page 3849), while the proposed regulations, themselves, provide for a 60 day period. (Page 3961 at 38 CFR §3.276(e)(5)(ii)).
 Comments may be submitted via email to http://regulations.gov. They should reference that they are in response to RIN-2900-AO73, “Net Worth, Asset Transfers, and Income Exclusions for Needs-Based Benefits”.

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