Neurology Clerkship UWORLD

Brain Tumours;
Epidemiology; median age 60, will have unilateral or bilateral associated with NF
Clinical manifestations; there is sensorineural hearing loss and inbalance (VIII) and facial
numbness/paralysis
Diagnostics; this will be done with audiogram and MRI with internal audatory canal
Management; observation, surgery and radiation
- Assymetric sensorineural loss; this will have air conduction, bone conduction and
lateralization with facial numbness----

CNVIII; this will be composed of cochlear nerve and vestibular nerve; inbalanece can occur and
it wil involve numbness due to CN VII involvement

Brain tumours; these are most consistent with a frontal lobe tumour; they can be asymptomat
Cholestoma; this will be keratin mass in the middle ear; it will be conductive, bone conduction>
air conduction
Eustachian tube dysfunction; assymetric hearing loss
HZV; can cause hearing loss but it will be linked to severe pain and vesicular rash
Menierre disease; this will have spinning vertigo, hearing loss and aural fullness
Educational goal; unilateral sensorineural loss will show reduced facial sensation. Vestibular
schwannoma, a benign tumour of CNVIII

Brain tumours; can be asymptomatic ---with ICP causes papilledema---cognitive dysfunction,

(unprovoked first seizure)
- Cognitive dysfunction (impaired memory)

Abuiia (motivation) and loss of interest (anhedonia)---there will be frontal lobe damage

FTD; this will manifest in the frontal lobe it is characterized by exective dysfunction-----
hereditary component most common ages 50-70

Educational goals; ICP and unprovoked first seizures are concerning for brain tumours; may
cause personality changes, abulia and anhedonia

Ischemic Stroke:

Risk Factors for ischemic Stroke:

Acute cerebral accident; this will have risk factors such as HTN, this will promote elevated
shearing force on the intracerebral vascular endothelium that will accelerate thrombi formation
 - It will promote 4x the risk of CVA, even mild reductions in BP can diminish CVA risk

Less significant risk factors for CVA; HTN, smoking, and sedentary lifestyle
HTN; this will increase risk of stroke, more than other risk factors including
hypercholesterolemia, DM, smoking and a sedentary lifestyle

Normal pressure Hydrocephalus;

There will be gait instability with frequent falls, cognitive dysfunction; urinary urgency and
incontinence; there is also depressed affect (frontal lobe compression). UMN signs in lower
extremities
Diagnosis; there will be marked improvement in gait with spinal fluid Millie Fisher lumbar test;
MRI
Treatment; VP shunting

Normal opening pressure on LP; there will be SAH; trauma, and destruction of the arachnoid
granulation that is responsible for CSF resoroption
Presentation; incontinence, cognitive impairment and gait abnormalities;

In sum, NPH is characterzed by ventriculomegaly with normal opening pressure, will show
incontinence, cognitive impairment and gait abnormalities in early disease; it is secondary to
neurologic insults that result in arachnoid granulations

Hemorrhagic Stroke;
Risk factors; Vascular malformations (AVMs), aneurysm,
Hemotological abnormalities (hemophaelia, SCD)
Clinical features; headache, vomiting, seizures, focal neurological deficits and AMS
Management; supportive, and reduction of ICP

HHT; this is concerning for an AVM; these are isolated congenital anomalous weakness through
weak vessels with telangectasia and multiorgan (lung, brain and liver); there will be sudden
onset of headache, vomiting, increased ICP

CT: shows irregular hyperdense region with margins

Basal Ganglia Putaminal hemorrhage;

There will be BG putaminal hemorrhage, there will cause sudden focal neurological deficits that
worsen over minuts to hours; there will be affecting the adjacent internal capsule leading to
contralateral hemiparesis and hemianesthesia----as the hemorrhage expands; there will be
nausea/vomiting due to elevated ICP
- Hypertensive vasculopathy involves the small penetrating branches---leading to
formation of Charcot Bouchard

Lobar/cortical hemorrhage---this is the most common cause of lobar heorrhages in the elderly
SAH: there will be ruptured berry aneurysms; with thunderclap headache and hyperattenuation
Epidural hematoma; this will have head injury----Altered consciousness; headache, n/v

Educational goal

Subarachnoid Hemorrhage;
Overview; this will show a hypertensive patient that is associated with a severe thunderclap
headache; meningeal irritation (nausea/vomiting—photophobia; they are also likely to suffer
from saccular//berry aneurysms

Management; this will be done with CT scan without contrast.

It will reveal acute hemorrhage in the brainstem and the basal cisterns with bleeding in the
intrahemispheric cistern and those with negative head CT will have elevated opening pressure
and xanthochromia

Cerebral amyloid angiopathy; this is the second most common cause of ICH; caused by
abnormal b-pleated sheets.

Aseptic meningitis; this will have headache, nausea. Vomiting, photophobia, nuchal rigidity

Cerebral venous thrombosis; this will be linked to hypercoagulable states with headache,
confusion and focal neurologic defects- diagnosis with venography

Vertebral artery dissection; causes local pain due to cerebral ischemia; this will be linked to
lateral medullary wallenburg syndrome; with ipsilateral Horner syndrome

Educational goal; nontraumatic SAH: due to ruptured saccular aneurysm and is linked to a
thunderclap headache and symptoms of meningeal irriaiton (nuchal rigidity, photophia and
nausea

SAH: this is caused by a rupture of a saccular aneurysm; this will be caused by a suden onset of
severe headache, thunderclap, this will be accompanied by vomiting and photophobia with
brief LOC; management, noncontrast CT scan of the brain; there will be xanthochroma

Movement Disorders;
Parkinson Disease
Cardinal findings; bradykinesia, 4-6 hz testing tremor; or cogwheel rigidity
Suggest diagnosis; unilateral with craniofacial (mased facial expression, decreased eye blink,
visual (blurred vision and impaired upward gaze, MSK (micrographia, dystonia and myoclonus),
shuffling gait; stopped gait, postural instability, autonomic dysfunction, nonpsychiatric
depression, psychosis disturbed sleep and dementia

Recall; resting tremor, bradykinesia, and rigidity are consistent with PD; there will be
complicated psychiatric symptoms; this will have psychosis----
Management; pramiprexole and ropinrole will exasperate psychosis more than levodopa
DDx; Deliriub; this is an acute onset fluctuating disorder that occurs with medical illness,
pharmacologic intoxication or withdrawal
Dementia with Lewy bodies; REM sleep behavio, fluctuating cognition, parkinsonism

Educational goal; PD; will show bradykinesia, rigidity, and tremor with visual hallucinations.
Treatment is qith quietipaine and pimvaserin

Essential Tremor;
This will be associated with involuntary movements with a neurologic cause that improve with
distraction
- Functional tremor; this will have an abrupt onset and it will result in functional tremor
- Often spared
- Changeable; shifting tremor frequency----chase the tremor

Educational objective; psychogenic tremors; this will present with significant disability------
changeable or inconsistent features; not consistent with known tremor syndromes;

Spinal Cord Diseases

Spinal cord compression; there will be loss of sensation and signs of upper motor neuron
disease. Epidural abscess is a particular concern in the IV drug use community; there will be
UMN signs

DDx; Malignancy
Educational goal; spinal cord compression is a sign and symptom of UMN disease, includes
weakness, hyperreflexia and extensor plantar response.

Epidural Abscess:
Pathogenesis; this will be caused by staphylococcus aureus
- Thi will be a distant infection (cellulitis, joint/bone pain), or IVDU
- Classic triad; fever, focal severe back pain and neurologic findings (motor sensory loss;
bowel or bladder dysfunction and paralysis

Overview; there will be worsening focal back pain, radcular nerve pain, sensory motor or reflex,
and paralysis

Suspected cases; urgent spinal MRI to confirm diagnosis followed by surgery---this can have
neurological sequelae and death

Spinal Cord Compression;

Spinal injury; MVA, malignancy; infection
Signs/symptoms; worsening severe low back pain that is worse at night and at the recumbent
position; there will be hypoactive or absence; late signs; bilateral babinksi reflex; decreased
rectal sphincter tone and increased DTRs
Management; emergency MRI; IV glucocorticoids

Central Cord Syndrome;

Cervical Cord spondylosis; there wil be acute spinal cord injury; with hyperextension and
collision
- There is commonly upper extremity manifestation including weakness due to damage of
the a- motor neurons in the anterior horn; there is also pain temperature and sensory
loss. There is also reflex loss at the level of injury

Educational goal; central cord syndrome, this is post whip lash injury in older adults with
underlying central cervical cord causes upper extremity, motor, sensory and reflex abnormality.
LMN function is generally preserved

Dementias
Alzheimers Disease; there is early, insidious short term memory with language deficits and
spatial disorientation. There is also personality changes;
Vascular dementia; there is a stepwise decline, early executive dysfunction, cerebral infarction
FTD; there is early personality changes, apathy and compulsive behaviour
Dementia with Lewy Bodies; visual hallucinations, spontaneous Parkinsonism, fluctuating
congition and rapid eye movement with sleep behaviour disorder

NPH; there is ataxia in early disease, urinary incontinence, and dilated ventricles on
neuroimaging

Prion disease; behavioural changes, rapid progression, myoclonus and or seizures

Behavioural changes; this includes socially offensive behaviour, social withdrawal, and
hyperorality (apathy, lack of insight)
- There is a behaviour variant FTD

Prion Disease;
Clinical features; this will have rapidly progressive dementia, myoclonus, cerebellar signs, UMN
signs such as hyperreflexia, and extrapyramidal signs such as hypokensia and mood.sleep
disturbances

Findings; will show widespread atrophy of the cerebrum and cerebrullum, cortical
enhancement of the putamen and caudate/hocky stick sign
CSF: 14-3-3 protein and positive RT-QUic PCR
EEF; sharp triphasic synchronous discharges
Periodic sharp wave complexes; will have CJD; thre will be neurodegeneration and widespread
loss of neurons. There will be inexorable decline (loss of speech, loss of ability of self care less
than 12 months post diagnosis

Educational goal; CJD; this is a fatal prion disease with rapidly progressive dementia,
myoclonus, sleep disturbances, there is no effective disease modifying treatment
Headaches
Migraine; there will be abnormal activation of trigeminal nerve; triggers, sleep deprivation;
stress and menses; epidemiology; increased incidence in boys and irls until puberty

Migraine with Aura;

This will manifest with recurrent unilateral headaches linked to nausea and paresthesia; this is
called migraine with aura; it is an episodic neurological disorder with photophia,
nausea/vomiting; more frequently in women than in men
- There will be increased risk of ischemic stroke with estrogen and progesterone pill

Educational goal; migraine is an episodic neurologic disorder; severe, unilateral throbbing pain
with photophobia, phonophobia nausea and vomiting there is a aura that precedes headache

Opthalmology
CMV retinitis; This will be followed by a latent lifelong infection; there will be severe deficits in
cell mediated immunity due to the loss of CD4+ cells, < 100, there will be blurred vision, floaters
and photopsia;

Fundoscopy; will reveal yellow fluffy hemorrhaegic lesions

Management; valganciclovir; this will reduce risk of blindness and retinal detachment
Antiretroviral therapy should also be initiated

Educational goal; CMV retinitis; this is the most common end complication of CMV int hose
with advanced AIDS, there will be blurred vision, floaters and photopsia (sensation of flashing
lights), there will also be retinal detachment; treatment necessitates antiretroviral medication
to prevent recurrrance

Obstetrics and Gynecology;

Risk factors; inherited thrombophilia, protein C/S deficiency, factor V; there is also association
with pregnancy and post partum; OCPs, malignancy and infection
Clinical; headache, elevated ICP (vomiting, and papilledema), seizures, and encephalopth
Diagnosis; MRI of the brain with venography
Treatment; anticoagulation (heparin acutely)
Central venous thrombosis; this is a rare life threatening formation within the dural sinuses, it is
related to a prothrombotic state including inherited thrombophilias; it will obstruct dural
venous drainage from the blood brain barrier.
- It will manifest with elevated ICP and seizures, vomiting and headache worsened in the
morning
- Management; MR venography that will help visualize flow deficit
Central venus thrombosis; prothrombotic conditons (postpartum, elevated ICPs, seizure and
stroke; will be confirmed by viewing flow void or MR venography

Urge Incontience
Micturition Centers;
Cerebral cortex; it will maintain continence by blocking urination
Pontine micturition center; coordinates detrusor contraction

MS: this can cause urgency incontinence; there wil be impairment of the UMN (descending
corticospinal tracts are inhibited leading to a micturition reflex and a small overtly contracted
bladder;
Management; antimuscarinics
In sum, those with MS can manifest with urge incontinence due to loss of cortical inhibition.

Preeclampsia
Risk factors; nulliparity, obesity, pre-existing medical conditions such as SLE, chronic HTN,
multiple gestation and advanced maternal age
Definitions; there will be new onset HTN (SBP > 140, or DBP > 90 at > 20 weeks, proteinuria or
signs of other end organ damage

Management < 37 weeks and no severe featuees; expectant, > 37weeks delivery
PO Nifedipine and seizure prophylaxis with magnesium sulfate
- There will be a unilateral frontal headache, visual aura, vision loss; this will also have
HTN SBP > 140, DBP >90, can have severe features
BP; will cause acute elevations in dysregulated cerebral blood flow; management labetolol

Educational goal; preeclampsia with severe features > 20 weeks with SBP > 140, and DBP > 90
with vision changes (blurry vision)

Psychiatry
Extrapyramidal Symptoms; Patient presents with worsening restlessness, wandering and
inability to sit still; this is suggestive of akathisia---there will be an inability to sit still; especially
in those with dementia who have limited verbal communication;
- Step 1 in management; dose reduction test; drug choice, propranolol or benzodiazepine
trial; if antipsychotic cessation is not an option; then a different antipsychotic
medication should be used
Antipsychotic; this will treat behavioural disturbances but it can cause akathisia; this is an
inability to sit still; management; dose reduction trial

Conversion Disorder; (functional neurological symptom disorder)

Clinical features; neurological symptoms; weakness, paralysis, nonepileptic seizures---not
intentionally produed (contrary to factitious disorder or malingering
Symptoms cause severe functional impairment and its precipitating
- This will be caused by relationship conflicts; or other stressors and support for patients

Antidepressents;
MDD; there will be MDD and worsening diabetic neuropathy; this is distressing and a disabling
complication that can exasperate depression, sleep disturbance and SNRI, duloxetine is shown
to have efficacy for depression and is the preferred choice in this patient

Educational goal; SNRI; duloxetine has analgesic properties for comorbid depression and
chronic pain and this includes painful diabetic neuropathy

CJD;
This will be a rapidly progressive dementia with myoclonus; cerebellar signs, UMN signs such as
hyperreflexia; extrapyramidal signs and mood/sleep disturbances
Findings; MRI; will reveal widespread atrophy; cerebellum and cerebrum
- MRI will show widespread atrophy (cerebrum and cerebellum; cortical enlargement and
caudate head---CSF 14-3-3 titers
- EEG; sharp triphasic synchronous discharges with spongiform degeneration without
inflammation

CJD: this will be an abnormal folded protein prion; this is promoted by startile with
noninflammatory neurodegeneration

RT-QIC tet can also be done

CKD; this is a fatal prion diseae with rapidly progressive dementia, personality changes visual
cortex degeneration, hypersomnia and myoclonus; fluorescent labeled proteins are the most
sensitive test

Medicine;
ESRD: this will have tingling, numbness and burning of the hands; suggesting CTS; there will be
compression of the carpel tunnel in the wirst; this is the most common mononeuropathy for
those on hemodialysis; this will be dialysis related; with increased venous pressure; blood
tracking; there will also be risk for ischemic neuropathy---note that symptoms worsen during
dialysis; it is reproducible with provocative measures

Educational goal; CTS; this is the most common mononeuropathy with ESRD with pain and
paresthesia; this will worsen during dialysis and more sever ein the arm with vascular access

IIH: (idiopathic intracranial HTN);

The patients presentation suggests increased ICP, optic nerve sheath rsulting in swelling of the
optic nerve head that will be visualized as papilledema on exam;
- There will be a blind spot on the visual fields at the location such as those with
papilledema---this will be secondary to increased ICP
Amaurosis Fugax; this will be transient monoopthalmic vision loss (blindness in the ophthalmic
artery)
Cataracts; this will have gradual vision loss
Glaucoma; this will have increased IOp
Optic neuritis; this will be associated with MS

Papilledma; this will be linked to increased ICP and have transient vision loss relative to head
position---there will be diagnostic evaluation, ophthalmic examination and persistent
papilledema can manifest with vision loss

Wernike Korsakoff Syndrome

This is associated with chronic alcoholism, malnutrition, hyperemesis gravidarum; thiamine
deficiency
Pathophysiology; thiamine deficiency;
Clinical features; encephalopathy, oculomotor dysfunction, nystagmus, postural and gait ataxia
- There is encephalopathy, oculormotor dysfunction, nystagmus
- Postural and gait ataxia

There will be long term thiamine and B1 deficiency; there is a high rate of intake, therefore we
administer glucose before thiamine

In sum, thiamine deficiency will cause wenike encephapathy

-

Idiopathic Intracranial HTN:

Risk factors; obese women of childbearing age; medications such as retinoids, tetracycline sand
growth hormones
Clinical features; headache, vision loss, enlarged blindspot, pulsatile tinnitus, diplopia, and
papilledema
Diagnosis; neuroimaging, LP (elevated opening pressure)
Management; weight loss and acetazolamide,
IIH; this is most common in obese women of childbearing age; thee will be positional headaches
which raise ICP; pulsatile tinnitus will also occur, this will manifest as optic disc edema
- Diagnosis; with MRI; will reveal elevated opening pressure in the brain.
Educational goal; IIH; this is most common in obese women of childbearing age that will
present as pulsatile tinnitus, and papilledema; diagnosis is with MRI and then LP

Polyarteritis Nodosum;
Pathophysiology; underlying Hep B and C; there is fibrinoid necrosis of the arterial wall with
intimal narrowing and interal/external lamina damage with microaneurysms
Clinical features; fever, weight loss and malaise
Diagnosis; negative ANCA and ANA
Angiography; microaneurysm and segmental/distal narrowing with nongranulomatosis and
transmural inflammation; there will be mononeuritis multiplex; with underlying vasculitis;
- There is assymetric polyneuropathy

Skin involvement; livido reticularis; renal insufficiency and abdominal pain; there will be elev
ESR

PAN; this will have mononeuritis multiplex with ?2 noncontigous findings with skin renal and GI
manifestations with sparing of the lungs

Heat Stroke;
Risk factors; strenuous activity during hot and humid weather; there is dehydration and poor
acclimization, lack of physicial fitness and obesity is another risk factor;
Clinical featues, core temp > 40, organ and tissue damage is also present, DIC, coagulation and
ARDs
Management; rapid cooling in ice water, high flow old water, fluid resuscitation and electrolyte
correction, no rle for antipyretic therapy
EHS; this is a temp > 40, there is CNS dysfunction, nonexertional headt stroke; must remove
from hot environment
Complications are DIC, end organ dysfunction---management, ABCs, fluid resuscitation and
treatment of end organ dysfunction
Educaitonal goal; heat stroke > 104, with CNS dysfunction (hot humid enviornments when
performing extreme activites such as DIC and end organ dysfunction

Emergency Medicine;
This seizure behaviour is associated with forceful eye closure and absence of self injury
consistent with psychogenic nonepileptic seizure
- This will have forceful eye closure, rapid alerting, orienting and immediate memory
recall; this will manifest in crowds
Labs; there will not be associated abnormal cortical activity;
Diagnosis; video EEG

Psychogenic nonepileptic seizure; this will have forced eye closure side-side head/body
movement and post ictal confusion; the gold standard is video eeg which will not show
epileptiform activity

Carbon Monoxide Poisoning;

Epidemiology; there will be caused by smoke inhalation; defective heating systems and gas
motors in poorly ventilated areas
Mild/moderate; headache, confusion, malaise, dizziness, nausea, severe, syncope and coma
Diagnosis; ABG; carboxyhemoglobin, ECG and cardiac enzymes
- Management 100% high flow O2 and intubation
- There will be cerebral hypoperfusion, dizziness and confusion, can have MI, seizures
(shown with tounge biting) coma and death
- Diagnosis; co-oximetry of ABGs
- Carbon monoxide; this is due to faulty indoor heating systems; there will be cerebral
hypoxia, headache, confusion, coma and death with elevated carboxyhemobloin levels

Pediatrics
Vitamin K; this is a cofactor in 2, 7,9 10; there will be poor placental transfer, absent gut glora,
poor vitamin K use, intramuscular K; there will be exclusively breast fed; there will have
hyperdense fluid collection in the posterior ventricles;---vomiting, irritability, bradycardia with
bulging fontanelle, rapidly enlarging head circumference with downward gaze

Newborns who do not obtain IM vitamin K are at risk of bleeding, ICH, there will be onstructive
hydrocephalus and signs of increased ICP; irritability, vomiting, bradycardia and HTN

Fragile X Syndrome (Trinucleotide CGG repeats; gene methylation silences FMR production
Gene methylation silences FMR production
Neuropsychiatric issues; developmental delay, intellectual disability, ADHD, ASD< self injurious
behaviour and anxiety
Examination findings; long face with prominent forehead, large protruding ears, macroorchism,
macrocephaly
Diagnosis; FMR1 DNA analysis

Other neurodevelopmental disorders

Rett Sydnrome; progressive brain detoriation that leads to microcephaly and developmental
regression; this in MECP2; in women, fatal in boys

Surgery
TBI management
1. Maintain MAP isotonic fluids and pressors
2. Reduce ICP; head elevation, sedation, osmotic therapy
3. Desmopressive intervention---CSF remova and craniectomy
Prevent ICH; can use TXA; reversal of anticoagulation
Other measures; prevent seizures; leveteracitam, phenytoin, control blood glucose Insulin 140-
180 and maintainance of normothermia (antipyretics and surface cooling)
TXA; antifibrinoltuc; this will be beneficial for mild TBI or severe TBI

In sum, acute traumatic coagulability; will have hypercoagulability and hyperfibrinolysis; with
antifibrinolytic therapy to enhance outcomes with moderate bleeding post hours after injury

Traumatic Injury to the left eye;

There will be inflammation, conjunctival erythema; this is most consistent with sympathetic
opthalmia; an AI disease where the eye is sensiztied to previously unsensitized antigens; there
will be an inflammatory response; management eye is enucleated to halt blindness

Neurocutaneous Syndromes;
NFII: this is localized on chromosome 22 and it encodes Merlin (there is variable expressivity at
ages 20-30)
Clinical manifestation; vesticular schwannoma, intracranial meningioma,, spinal tumours,
cataracts and cutaneous plaques or tumours
Mangement; surveillance, audiogram and MRI

NFII: will have > 95% develop sensorneural hearing loss, it is an AD defect (merlin)

NFI: this is an AD neurocutaneous syndrome with café au lait spots and cutaneous
manifestations appearing in infancy; there will be done with increasing age, axillary/inguinal
frecles and neurofibromas
- Positive optic glioma, this will also have headaches and decreased visual acuity with
morning headache,
- Managemnet; 1. MRI of the brain and orbits

NF2; this will have acoustic neuromas bilaterally; this can lead to sensorineural hearing loss;
ESR; this is an acute phase reactant in the setting of inflammation
LP; this will rule out meningoencephalitis

Educatioal goal; this will have optic pathway gliomas, decreased visual acuity and MRI of the
brain and orbits evaluate for an intracranial mass.

Infectious Diseases;
Brain abscess; there is risk for mastoiditis; dental infection, cyanotic heart disease---
- Cyanotic congenital heart disease (TOF), this will raise the risk for brain abscess; this will
cause a right to left shunt----
- Headache; will have vomiting particularly in the morning; there is a fever and focal
neurological changes
Hypocalcemia; this is a common featue of Digeorge; however, it will not explain the fever

Educational objective; there will be headache, fever, focal neurologic deficits and seizures;
there is a risk for brain abscess due to bacterial spread

HSV Encephalitis;
Clinical features; fever, headache, seizure, AMS (Confusion agitation)
Focal neurologic findings (hemiparesis, craial nerve palsies)
Diagnostic findings; elevated WBC, RBC, protein and normal glucose
Treatment; IV acyclovir
- There will be seizures/fever, AMS and focal neurologic findings----HSV there will be
changes in the trigeminal ganglion with hemorrhage and edema
Reye syndrome; this will have liver dysfunction, will preent with generalized seizures post viral
illess

AMS; fever, headaches, seizure, temporl lobe abnormalities and edema are highly suggestive of
HSV encephalitis

Sleep Disorders;
Narcolepsy; there will be recurrent lapses into sleep/naps > 3 times a week for 3 months; there
is cataplexy; brief loss of muscle tone precipitated by strong emotion (such as excitement) );
associated features hypnagogic or hypnopompic hallucinations and sleep paralysis
- There is cataplexy; this is transient loss of muscle tone in response to intense emotion,
this is suggestive of REM sleep phenomena and seel paralysis s
- There will be low levels of orexin; hypocretin 1

Narcoplesy; excessive daytime sleepiness, cataplexy and REM sleep related phenomena with
hypnagogic and hypnopompic hallucinations