Term
| Symptoms of Progressive bulbar palsy |
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Definition
| tongue & palate weakness; pts may later develop ALS |
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Term
| W-H disease: muscle biopsy |
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Definition
|
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Term
| A baby with W-H disease has a characteristic “forg-leg posture” that is due to |
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Definition
|
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Term
|
Definition
|
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Term
| K-W disease: SMN mutation |
|
Definition
| SMN1 – absent|SMN2 – large |
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Term
|
Definition
|
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Term
| Causes of delayed sleep onset in Secondary insomnia |
|
Definition
| anxiety, physical activity, jet lag, shift work, sedative withdrawal, stimulant use |
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Term
| Peak levels of Melatonin at |
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Definition
|
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Term
| EEG frequencies, amplitudes: |
|
Definition
| β, α, θ, δ(< 13 Hz, < 5 mV), (8 -13 Hz, 5-15 mV), (4-7 Hz, 10-50 mV), (< 4 Hz, > 50 mV) |
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Term
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Definition
|
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Term
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Definition
|
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Term
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Definition
|
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Term
| decreased light sends electrical signals to |
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Definition
| suprachiasmatic nucleus (master clock) → activation of ? → activation of pineal gland & release |
|
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Term
|
Definition
| glutamate antagonists, anticholenergics and other symptomatic treatments such as stool softeners, antispastics, botulinum toxin, antidepressants, bracing, gastrostomy for feeding, ventilation) |
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Term
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Definition
|
|
Term
| as sleep progresses…frequency? Amp? |
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Definition
| frequency SLOWS and amplitude INCREASES |
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Term
| A horizontal section of the spinal cord of an ALS patient would reveal |
|
Definition
| A lack of myelin in the corticospinal tracts and a loss of anterior Horn neurons |
|
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Term
| REM appears very similar to what state on EEG |
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Definition
|
|
Term
| Cholinergic Circuit|Cholinergic neurons from (1)_________ and (2)__________ nuclei → (3)______ and other brainstem areas → activation of (4)______ pathways → (5)___frequency, (6) ___amplitude EEG activity (7_) ⇒ arousal and alertness |
|
Definition
| Cholinergic neurons from (1)pedunculopontine (PPT) and (2)lateral dorsal tegmental (LDT) nuclei → (3)thalamus and other brainstem areas → activation of (4)thalamic-cortical pathways → (5)high frequency, (6)low amplitude EEG activity (7β) ⇒ arousal and alertness |
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Term
| Sleep walking and night terrors occur in what stage? |
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Definition
|
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Term
| stage III has what activity |
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Definition
|
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Term
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Definition
|
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Term
| Sleep stage II characteristics |
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Definition
| sleep spindles and K complexes; conscious awareness of the environment disappears |
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Term
|
Definition
| neurons in superior cervical ganglia |
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Term
| Trp product that stimulates a drowsy state by modulating brainstem neurons to facilitate onset of sleep |
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Definition
|
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Term
| Cholinergic pathway is active |
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Definition
| when awake and during REM |
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Term
| Early in sleep, NREM stages |
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Definition
|
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Term
| Towards the morning…NREM vs REM |
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Definition
|
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Term
| REM sleep: metabolism HR, RR, BP, body temp |
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Definition
|
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Term
| A 40 yr women presents to clinic with weakness indicative of a lower motor neuron disease and peripheral neuropathy she describes as “steadily getting worse over the past year”. You get a muscle biopsy in which you see a characteristic accumulation on the nerves. This pt has |
|
Definition
| polyclucosan body disease – glycogen storage disorder that characteristically presents in younger individuals; muscle or nerve biopsy will show accumulation of intracellular polyglucosan bodies that are found throughout the pt nervous system |
|
|
Term
| The differential diagnosis of ALS includes |
|
Definition
| (1) Multisystem atrophy| (2) hereditary cerebellar degeneration|(3) tumors of the craniocervial junction|(4) spondylosis|(5) poliomyelitis|(6) polyglucosan body disease |
|
|
Term
| Secondary RBD can be caused by |
|
Definition
| alcohol withdrawal, TCA & SSRI use |
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|
Term
| Causes of delayed sleep onset in Primary insomnia |
|
Definition
| idiopathic or psychophysiologic |
|
|
Term
| Patient presents with dysphagia and ataxia |
|
Definition
| Hereditary cerebellar degeneration |
|
|
Term
| Pt presents with symptoms of ALS but has a Hx of polio in childhood. You therefore consider |
|
Definition
| progressive LMN disease due to degeneration of the neurons that survived the childhood disease |
|
|
Term
| Pt presents with progressive muscle weakness that causes you to include ALS in your differential. But labs come back with elevated serum calcium. Pt most likely has |
|
Definition
| parathyroidism that has not yet been diagnosed. Elevated PTH blood levels is diagnostic |
|
|
Term
| Physical exam reveals generalized weakness, hyperreflexia and spasticity but normal sensation. Pt has no significant PMHx or FHx. Diagnosis? Amyotrophic lateral sclerosis: MOA of ALS |
|
Definition
| progressive and LETHAL degeneration of upper and lower motor neurons; most cases are sporadic with only 10% being hereditary |
|
|
Term
| 5 diseases that are α-synucleinopathies |
|
Definition
| Parkinson’s, multisystem atrophy, Lewy body dementia, Progressive Supranuclear Palsy |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
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Term
|
Definition
| days to weeks while chronic is > 6 weeks |
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|
Term
| Causes of delayed sleep onset in Primary insomnia |
|
Definition
| idiopathic or psychophysiologic |
|
|
Term
| Causes of delayed sleep onset in Secondary insomnia |
|
Definition
| anxiety, physical activity, jet lag, shift work, sedative withdrawal, stimulant use |
|
|
Term
| REM sleep behavior disorder |
|
Definition
| loss of atonia/paralysis during REM sleep leading to physical acting out of dream states including verbalization, punching, kicking |
|
|
Term
| REM sleep behavior disorder is most common in |
|
Definition
|
|
Term
| 5 diseases that are α-synucleinopathies |
|
Definition
| Parkinson’s, multisystem atrophy, Lewy body dementia, Progressive Supranuclear Palsy |
|
|
Term
| Insomnia has a strong association with |
|
Definition
|
|
Term
| Pt presents with arm and hand atrophy, weakness and spasticity from compression of the pyrimdal tracks. There is minimal sensory loss. You are suspicious of ALS but before making your diagnosis you call for |
|
Definition
| an MRI of the pt spine to rule out a degenerative disc such as cervical spondylosis which |
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|
Term
| Male pt presets with CC of recurrent muscle cramps and generalized weakness. Physical exam revelas trophy, fasiculations, signs of denervation in limbs and tongue as well as mind neuropathy. There is no significant PMH or FH. Labs reveal a slightly elevated serum CPK. What test should you call for now? |
|
Definition
|
|
Term
| Test results reveal a mutation of the androgen receptor on the X chromosome. This man has |
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Definition
|
|
Term
| Secondary RBD can be caused by |
|
Definition
| alcohol withdrawal, TCA & SSRI use |
|
|
Term
| Myopathies can be distinguished from ALS by |
|
Definition
| Myopathies can be distinguished from ALS by serum CPK (↑ in myopathies), EMG, & muscle biopsy |
|
|
Term
| Microscopic findings of ALS |
|
Definition
| eosinophilic bunina inclusion bodies in cytoplasm of anterior horn neurons → ubiquitin protein accumulations |
|
|
Term
| ALS etiology: excitotoxicity |
|
Definition
| an increase of glutamate-mediated exocitotoxicity causes neuronal degredation |
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Term
|
Definition
| SOD mutation in chromosome 21 in AD familial ALS (only gene defect that is not rare) ⇒ toxic gain of function of the super oxide dismutase enzyme |
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Term
| REM sleep behavior disorder |
|
Definition
| loss of atonia/paralysis during REM sleep leading to physical acting out of dream states including verbalization, punching, kicking |
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Term
|
Definition
|
|
Term
| If a pt with Progressive lateral sclerosis were to develop ALS how would it manifest |
|
Definition
| would be a slower progression of symptoms |
|
|
Term
| Dopaminergic neurons from substantia nigra → cortex are important for |
|
Definition
|
|
Term
| Why should pt always have an MRI before a diagnois of ALS is made |
|
Definition
| could be tumors of craniocervical junction –pts present with arm weakness and dysphagia |
|
|
Term
| What remains unaffected in individuals with motor neuron disease |
|
Definition
| normal sensation, normal nerve conduction velocity |
|
|
Term
| Serotonergic neurons from dorsal and medial raphe nuclei → cortical centers have a pattern similar to |
|
Definition
| noradrenergic input to cortical centers| wakefulness >>>> NREM >> REM |
|
|
Term
| Noradrenergic input from locus ceruleus → neocortex:| wakefulness, NREM, REM |
|
Definition
| (highly active) wakefulness >>> NREM >> REM (silent) |
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|
Term
| REM:|• eyes|• muscles|• dream?|• sexual |
|
Definition
| • rapid, ballistic eye movement|• muscle paralysis|• vivid emotional dreams|• penile and clitoral erection |
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|
Term
| Light-dependent biological clock |
|
Definition
| ambient light reaches retinal ganglion cells containing melanopsin ⇒ inhibition |
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|
Term
| Sx of motor neuron disease: EMG |
|
Definition
| will indicate denervation and decreased number of motor units |
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|
Term
| Sx of motor neuron disease: muscle biopsy |
|
Definition
| atrophic fibers and fiber grouping |
|
|
Term
| ALS results in atrophy of |
|
Definition
|
|
Term
| ALS patients have a positive |
|
Definition
| Babinski sign (dorsiflexion in response to the plantar reflex in adults – normal response is plantarflexion) |
|
|
Term
| Hyperreflexia is characteristic of what type of lesion |
|
Definition
|
|
Term
| Sx of motor neuron disease: atrophy? |
|
Definition
|
|
Term
|
Definition
| Sleep is not.. an absence of all brain activity |
|
|
Term
|
Definition
| 7.5 h/night; sleep = 1/3 of lifespan |
|
|
Term
| Inheritance pattern of K-W disease |
|
Definition
| Autosomal recessive mutation of Survival motor gene |
|
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Term
|
Definition
| fatal – early death by respiratory failure |
|
|
Term
| Progressive bulbar palsy affects primarily muscles innervated by |
|
Definition
|
|
Term
| K-W disease clinically resembles |
|
Definition
|
|
Term
| Cholinergic pathways is inhibited |
|
Definition
| during NREM (thalamic-cortical pathways deactivated) |
|
|
Term
|
Definition
| group of cellular/molecular cycles inherent in a variety of organs that drive circadian rhythms |
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|
Term
|
Definition
|
|
Term
| Sympathetic nucleus that activates neurons in interomediolateral gray of upper spinal cord |
|
Definition
|
|
Term
|
Definition
| signs of denervation and fasiculations (tongue) |
|
|
Term
| 13 yo pt presents to clinic with arm hyperpronation, muscular atrophy, and fasiculations. Mother describes the symptoms as “slowly progressive.” What labs would you want to run on this pt |
|
Definition
| [serum CK|• if elevated⇒ Dx: myopathy (muscular dystrophy)|• normal⇒ Dx: Kugelberg Welander Disease |
|
|
Term
| Sx of motor neuron disease: weakness |
|
Definition
| symmetrical or asymmetrical weakness |
|
|
Term
| Sx of motor neuron disease: reflexes |
|
Definition
| increased or decreased reflexes depending on corticospinal tract involvement |
|
|
Term
| Sx of motor neuron disease: fasiculations? |
|
Definition
|
|
Term
| Inheritance pattern of Werdnig-Hoffman |
|
Definition
| Autosomal recessive (SNM mutation) |
|
|
Term
| Infantile spinal muscular atrophy is |
|
Definition
|
|
Term
|
Definition
| if pt has neonatal or juvenile form of spinal muscular atrophy |
|
|
Term
|
Definition
|
|
Term
| survival motor neuron gene (SMN) |
|
Definition
| Chromosome 51; 2 copies – SMN1 and SNM2 |
|
|
Term
|
Definition
|
|
Term
| Anterior horn cell disease may be |
|
Definition
|
|
Term
| Anterior Horn cell disease: reflexes |
|
Definition
| depressed reflexes (except ALS) |
|
|
Term
|
Definition
|
|
Term
| AHC disease: muscular manifestations |
|
Definition
| weakness, muscle atrophy, fasciculations |
|
|
Term
| Anterior horn cell disease: sensory deficits |
|
Definition
|
|
Term
| Histaminergic output from the tuberomamillary nucleus:| wakefulness, NREM, REM |
|
Definition
| high during wakefulness – LOWER during NREM – even LOWER during REM sleep |
|
|
Term
| Drugs that block H1 receptors |
|
Definition
| increase NREM and REM sleep (i.e.. Benadryl) |
|
|
Term
| What is the source of histaminergic input to cortical centers? |
|
Definition
| tumberomammillary nucleus |
|
|
Term
| Irresistible, daytime sleep onset |
|
Definition
|
|
Term
| Sx of Narcolepsy usually develop by the |
|
Definition
|
|
Term
| Narcolepsy may be secondary to |
|
Definition
| MS, pituitary tumors, vascular malformations, stroke |
|
|
Term
| The Pathogeneis of Narcolepsy is a loss of |
|
Definition
| hypocretin/orexin secreting neurons in the tuberomammillary nucleus of the thalamus |
|
|
Term
| Narcolepsy Tx: daytime sleepiness |
|
Definition
| methylphenidate, modafinil, γ-hydroxybutyrate |
|
|
Term
| Loss of hyocretin/orexin secreting neurons is typically related to what 2 pathogenic states |
|
Definition
| (1) HLA genes that predispose pt to an autoimmune attack on the neurons|(2) secondary to a tumor, stroke, etc that results in loss of these neurons |
|
|
Term
| Narcolepsy is excessive daytime sleepiness associated with |
|
Definition
| One or more of the following tetrad:| (1) sleep attacks/intrusions|(2) cataplexy|(3) sleep paralysis |(4) hypnagogic hallucinations |
|
|
Term
| persistent REM paralysis after awakening |
|
Definition
|
|
Term
| abrupt loss of muscle tone during waking hours |
|
Definition
|
|
Term
| dream persistence after awakening |
|
Definition
|
|
Term
| prevalence of narcolepsy symptoms |
|
Definition
| EDS > cataplexy > hypogogic hallucinations > sleep paralysis |
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|
Term
| How do we transition between REM and NREM sleep |
|
Definition
| fluctuation between REM-ON cells and REM-OFF cells; whichever activity predominates over the other dictates the state we are in |
|
|
Term
| Airway obstruction seen in sleep apnea is the result of complex interaction between what 3 structures |
|
Definition
| pharyngeal muscles, tongue, & soft palate |
|
|
Term
|
Definition
| excessive daytime fatigue, snoring, heartburn, memory loss, irritability, depression, morning headache, dyspnea, nocturia, impotence |
|
|
Term
| nasal obstruction, tonsillar/adenoid hypertrophy, macroglossia, reflux laryngitis, thick neck, hypothyroidism/goiter, CHF, pitting edema are all |
|
Definition
| physical findings of Obstructive sleep apnea |
|
|
Term
|
Definition
| self-reported tendency to fall asleep in 8 different situations, situations depending on soporific nature of each pt |
|
|
Term
| excessive daytime sleepiness as defined by Epworth sleepiness scale |
|
Definition
| tendency to fall asleep in > 9 situations |
|
|
Term
| Multiple sleep latency test looks at |
|
Definition
| EEG defined sleep latency during 4-5 daytime naps |
|
|
Term
| cytokines that promote sleep |
|
Definition
|
|
Term
|
Definition
| excessive daytime sleepiness, insomnia, snoring, abnormal behavior, nightmares, abnormal movements |
|
|
Term
| melatonin secretion by pineal gland is turned on by |
|
Definition
|
|
Term
| Lack of adequate sleep results in increased |
|
Definition
|
|
Term
|
Definition
| repetitive blockage of respiratory pathway during sleep causing apneic periods lasting longer than 10 s and causing oxyHb desaturations > 4%; |
|
|
Term
| increased incidence of obstructive sleep apnea in (4) |
|
Definition
| (1) men|(2) obese individuals|(3) HTN|(4) heart disease |
|
|
Term
| endogenous sleep-promoting chemicals that accumulate during wakefulness and promote sleep onset |
|
Definition
|
|
Term
| Adenosine accumulates in CNS during |
|
Definition
| wakefulness [and declines during sleep] |
|
|
Term
| What is the mechanism of Myasthenia Gravis that makes it a postsynaptic NMJ disorder |
|
Definition
| MG is an autoimmune disorder in which individuals make autoantibodies to their OWN post-synaptic Ach receptors. These autoAbs cause Ach blockade, Ach receptor destruction (comp-mediated) and ↑rate of Ach degradation |
|
|
Term
| T/F: the CMAP of a MG pt will not be affected by fast repetitive stimulation |
|
Definition
| Which is indicative of these pt ability to maintain tonic contraction and thus fatigue quickly |
|
|
Term
| CMAP amplitude of your pt DECREASES following slow repetitive stimulation. Pt most likely has what disorder |
|
Definition
| POSTSYNAPTIC NMJ disorder (i.e., Myasthenia Gravis) |
|
|
Term
| MOA of decreased CMAP amplitude under repetitive stimulations… |
|
Definition
| MOA of decreased CMAP amplitude under repetitive stimulations In myasthenia gravis the number of quanta and quanta released are normal. But due to decrease in ACh receptor the same quanta generates only a small EPP and the safety factor is reduced ∴ ↓ EPP ⇒ ↓ individual Muscle APs generated ⇒ ⇒ decline in CMAP amplitude and area which correlates with… muscle weakness which progresses throughout the day |
|
|
Term
| PRESYNAPTIC NMJ disorders aka “lambert-eaton syndrome” the CMAP amplitude is |
|
Definition
| LARGER following fast stimulation….WHY? in lambert eaton the problem is an inability to release ACH from pre-synaptic bouton ∴ as the number of stimulations increases the amount of ACH released will also increase ⇒ CMAP amplitude will increase as well |
|
|
Term
| Slow Channel response to repetitive muscle stimulation |
|
Definition
| Decremented response of compound muscle after repetitive stimulation. Why…? All Ach receptors are saturated as a result of Ach increased affinity. Also, the persistently opened Na channels result in increased Ca2+ influx ⇒ destruction of the end plate. |
|
|
Term
| What are 3 general characteristics of see in MG pts |
|
Definition
| (1) ptosis that increases with sustained upwards gaze|(2) Possible diplopia|(3) proximal limb weakness |
|
|
Term
| Pathophysiology of L-E syndrome that results in its classification as a PRE-synaptic disorder |
|
Definition
| autoantibodies block the release of Ach from presynaptic bouton via blockade of presynaptic calcium voltage channels (NMJ--nicotinic effects). |
|
|
Term
| Pt presents to clinic and after doing a physical exam you suspect Lambert-Eaton syndrome. Why would you want to get a chest X-Ray? |
|
Definition
| Pt presents to clinic and after doing a physical exam you suspect Lambert-Eaton syndrome. Why would you want to get a chest X-Ray? 60% of patients with LEMS have an underlying malignancy that is most often small cell lung cancer |
|
|
Term
| Middle-aged female pt presents to clinic in the late afternoon. She came straight from work. As soon as you walk in the room and see her you know she has Myasthenia Gravis. How? did you know this? |
|
Definition
| The patient had ptosis and a visible thymoma (enlarged thymus glad) |
|
|
Term
| After you get a full patient history but before you perform a physical exam you are fairly certain this pt MG is in the end stages of the dx. What part of her HPI makes you think this |
|
Definition
| Pt reported have difficulty swallowing and breathing |
|
|
Term
| You perform a single fiber EMG on a pt you suspect of having early onset MG but you are not entirely sure. Why this test? |
|
Definition
| It is the most sensitive test for diagnosing MG |
|
|
Term
| If the pt did have MG how would their SFE results differ from those of a normal individual? |
|
Definition
| Normally there is small variation but overall same wave patter of transmission between the two fibers||in MG pts variable and absent potentials are evident proving impaired neuromuscular transmission |
|
|
Term
| Pt presents with obvious signs of a NM transmission disorder. During the physical exam you notice the pt mouth is abnormally dry and their pupils are small and poorly reactive. Dx? |
|
Definition
|
|
Term
| Why would decreased salivation and constricted non responsive pupils be indicative of LEMS? |
|
Definition
| LEMS affects not only neuromuscular transmission via (nicotinic receptors) but also autonomic synaptic muscarinic receptors |
|
|
Term
| Autoantibodies of MG vs LEMS |
|
Definition
| in MG the autoAbs affect ONLY nicotinic receptors⇒ NO defects of the sympathetic system||in LEMS autoAbs affect BOTH nicotinic (NMJ) AND muscarinic receptors located at the autonomic ganglia synapses |
|
|
Term
|
Definition
| repetitive stimulations test serum autoantibodies, and Single fiber Electromyography |
|
|
Term
| CC: vision loss sometimes see double when really tired plus an overall feeling of fatigue at the end of the day |
|
Definition
|
|
Term
|
Definition
| LEMS Tx neoplasm removal, cholinesterase inhibitors for symptomatic relief, immunosuppressive therapy such as corticosteroids. |
|
|
Term
| what test would you use to determine if a pt with MG symptoms actually has the dz? |
|
Definition
| what test would you use? Administer an anticholinesterase drug like Edrophonium ⇒ no effect on muscle fatigue = CMS; visible difference i.e., decreased ptosis = MG |
|
|
Term
| Response to exercise: MG vs LEMS while both patients would shows signs of fluctuating muscle weakness a MG pt would have increased muscle fatigue following exercise while a LEMS pt would show improvement in muscle |
|
Definition
| strength and tone following exercise |
|
|
Term
| On entering your patients examination room he tries to stand up to greet you. However your astutely observant neurologist eye notices that although he hides it well the pat had some difficulty rising from the chair. You immediately add what to the top of your differential |
|
Definition
|
|
Term
| When testing your pts muscle stretch reflexes their response leads you to a differential diagnosis of Lambert-Eaton syndrome. Describe their reflexive response? |
|
Definition
| Initially pt exhibits areflexia but with a few repetitive taps the muscle stretch reflex improves and there is some response |
|
|
Term
| What is a paraneoplastic syndrome? |
|
Definition
| a condition that arises as a result of cancer elsewhere in the body |
|
|
Term
|
Definition
| Drugs in this class work to increase the amount of Ach available in the synaptic terminal (↓ degredation by AchE) ⇒ increased chance for Ach to outcompete the autoantibodies bound to postsynaptic receptors ⇒ generate stronger EPP |
|
|
Term
| CC: difficulty climbing stairs to apartment and generalized weakness especially in the legs |
|
Definition
|
|
Term
|
Definition
| anticholinesterase, immunotherapy, corticosteroids or thyrectomy |
|
|
Term
| How do corticosteroid and or a thyrectomy alleviate Sx in a pt with MG |
|
Definition
| help decrease the production of autoantibodies |
|
|
Term
| Pathophys of Congenital Slow Channel Syndrome |
|
Definition
| Neuromuscular transmission is affected by an increased affinity of Ach for its receptor resulting in prolonged attachment of NT to receptor. This results in… prolonged opening of Na+ channels and a longer depolarization period |
|
|
Term
| Etiology of Slow Channel Syndrome |
|
Definition
| AD heritable (LEMS and MG are acquired autoimmune disorders) |
|
|
Term
| compound muscle action potential amplitude (CMAT) for normal muscle |
|
Definition
|
|
Term
|
Definition
| quinidine (antiarrythmic drug that blocks Na channels) or Prozac |
|
|
Term
| Why cant you treat Slow Channel syndrome with Anticholinesterases |
|
Definition
| these individuals will NOT benefit from this class of drugs; the problem in Slow Channel Syndrome is an inherited increased affinity of Ach for its receptor ∴ increasing the amt of Ach available to bind will have no effect |
|
|
Term
| Who would benefit from the effects of anticholinesterases? |
|
Definition
|
|
Term
| In general the best way to diagnose a NMJ disorder is via |
|
Definition
| Stimulation nerve test (applicable for BOTH pre and postsynaptic disorders) |
|
|
Term
| The lateral hypothalamic areas are a source of |
|
Definition
|
|
Term
| A lesion of the VLPO of the hypothalamus results in |
|
Definition
|
|
Term
| Nuclei activity during REM sleep |
|
Definition
| same as NREM except increased PPT/LDT activity at beginning (REM ON) while locus ceruleus activity increases at the end (REM OFF) |
|
|
Term
| Activation of what creates the EEG pattern of REM |
|
Definition
|
|
Term
| The atonic paralyzed state that accompanies REM sleep is the result of |
|
Definition
| REM-ON cell activation of medullary brainstem centers → glycine-mediated inhibition of anterior horn cells in the spinal cord |
|
|
Term
| What nuclei when activated induce arousal (there are 7) |
|
Definition
| (1) PPT|(2) LDT|(3) locus ceruleus|(4) sustantia nigra|(5) raphe nuclei|(6) tuberomammillary|(7) lateral hypothalamus |
|
|
Term
| Nuclei activity during wakefulness |
|
Definition
| decreased VLPO|increased all other hypothalamic and brainstem nuclei |
|
|
Term
| Nuclei activity during NREM sleep |
|
Definition
| increased VLPO| decreased all other hypothalamic and brainstem nuclei |
|
|
Term
| Orexin/hypocretinneurons in lateral hypothalamus project to the forebrain where they |
|
Definition
|
|
Term
| 90% of pts w/narcolepsy have decreased or absent levels of |
|
Definition
| orexin and ↓orexin secreting neurons |
|
|
Term
| the ventrolateral preoptic nucleus (VLPO) of hypothalamus contains |
|
Definition
| GABAergic and Galanin neurons |
|
|
Term
| GABAergic and Galanin neurons |
|
Definition
| innervate and INHIBIT arousal nuclei |
|
|
Term
| Activation of VPLO results in |
|
Definition
| ↓forebrain arousal ⇒ onset and progression of NREM sleep through its 4 stages |
|
|
