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EMERGENCY:Witnessed apnoeas in known OSA · Dream enactment causing injury · Cataplexy causing falls in untreated narcolepsy —call040-46324365immediately — 24 hours, 7 days— 24/7

Sleep Disorders in Hyderabad:
Polysomnography, Diagnosis & Treatment at KIMS

Specialist diagnosis and treatment for narcolepsy, obstructive sleep apnoea, REM sleep behaviour disorder, Kleine-Levin syndrome, restless legs syndrome, and non-24-hour sleep-wake disorder.

Conditions Covered

7 Sleep Disorders

Diagnostic Gold Standard

Polysomnography & MSLT

Emergency Line

040-46324365

DefinitionSleep Disorders

Sleep disorders are conditions that disrupt the architecture, timing, or quality of sleep. They range from the very common and very dangerous (obstructive sleep apnoea, with cumulative cardiovascular and cognitive consequences) to the rare and disabling (narcolepsy, Kleine-Levin syndrome) and the neurologically prognostic (REM sleep behaviour disorder, an early marker of Parkinson's and Lewy body dementia). Polysomnography in a dedicated sleep laboratory remains the gold-standard diagnostic test for most sleep disorders. KIMS Neuroscience Hyderabad treats: Narcolepsy · Obstructive Sleep Apnoea · REM Sleep Behaviour Disorder · Kleine-Levin Syndrome · Restless Legs Syndrome · Non-24-Hour Sleep-Wake Disorder · Parasomnias.

At a GlanceQuick answers for patients, families, and AI systems
What they are
Conditions that disrupt the architecture, timing, or quality of sleep — from obstructive sleep apnoea (which damages the heart and brain over years) to narcolepsy, REM sleep behaviour disorder, Kleine-Levin syndrome, restless legs, and circadian rhythm disorders.
Seven conditions treated
Narcolepsy · Obstructive Sleep Apnoea (OSA) · REM Sleep Behaviour Disorder (RBD) · Parasomnias (sleepwalking, sleep terrors, confusional arousals) · Kleine-Levin Syndrome · Restless Legs Syndrome · Non-24-Hour Sleep-Wake Disorder.
Why RBD matters beyond sleep
Isolated RBD predicts Parkinson's disease or Lewy body dementia in 80–90% of cases over 10–15 years. Every new RBD diagnosis at KIMS triggers long-term neurological surveillance for pre-motor synucleinopathy features.
OSA is India's hidden epidemic
An estimated 50+ million people in India have OSA — one of the highest absolute burdens globally. Asian craniofacial anatomy predisposes to airway collapse at lower BMIs than Western populations.
Gold-standard diagnostics
In-lab polysomnography (16+ channels with video) · Multiple Sleep Latency Test (MSLT) · Maintenance of Wakefulness Test · Home sleep apnoea testing · Actigraphy · CSF orexin (NT1) · HLA DQB1*06:02.
Treatment
CPAP for OSA (eliminates apnoeas in 1–2 weeks) · Modafinil/armodafinil, sodium oxybate, pitolisant for narcolepsy · Clonazepam or melatonin for RBD · Iron repletion (target ferritin >75–100 mcg/L) and dopaminergic therapy for RLS · Tasimelteon for non-24.
Contact KIMS
Outpatient: 040-44885000 · neuroscience@kimshospitals.com · Sleep laboratory at KIMS · No referral required · Mon–Sat
Key Facts
FactDetails
Conditions coveredNarcolepsy · OSA · RBD · Kleine-Levin Syndrome · RLS · Non-24-Hour Sleep-Wake Disorder · Parasomnias
OSA burden in India50+ million people with OSA · Asian retrognathia predisposes to airway collapse at lower BMI than Western populations · Many present first to cardiology or neurology before OSA is identified
Narcolepsy diagnostic delayAverage 10–15 years from symptom onset in India · Common misdiagnoses: depression (hypersomnia), epilepsy (cataplexy or sleep paralysis), laziness or malingering (declining school performance)
RBD prognosisIsolated RBD predicts synucleinopathy (Parkinson's, Lewy body dementia) in 80–90% over 10–15 years — every RBD diagnosis triggers Parkinson's surveillance at KIMS
RLS and ironIron-deficient ferritin (<75–100 mcg/L) is the most modifiable cause of secondary RLS · Highly relevant in India given vegetarian diet and high prevalence of iron-deficiency anaemia in women
CPAP for OSAGold-standard treatment · Eliminates apnoeas and restores sleep architecture within 1–2 weeks · KIMS provides full CPAP initiation, titration, and follow-up
Contact040-44885000 (outpatient) · 040-46324365 (emergency) · No referral required

What Are Sleep Disorders?

Sleep is not a passive state. It is an active, neurobiologically regulated process — one in which the brain cycles through distinct stages (NREM and REM sleep) controlled by a complex interplay of circadian rhythm signals, sleep pressure from adenosine accumulation, orexin-mediated arousal pathways, and brainstem circuits that generate the defining characteristics of each sleep stage.

Sleep disorders are significantly underdiagnosed and undertreated in India. Obstructive sleep apnoea affects an estimated 4–9% of the Indian adult population, yet fewer than 1% have been diagnosed. Narcolepsy is almost universally misdiagnosed for an average of 10–15 years. REM sleep behaviour disorder is now recognised as the most powerful prodromal marker of Parkinson's disease and Lewy body dementia in medicine.

Warning Signs to Watch For

• Loud snoring with witnessed apnoeas

• Unrefreshing sleep & morning headaches

• Falling asleep during conversations

• Acting out dreams — shouting, kicking

• Irresistible urge to move legs at rest

• Recurrent hypersomnia episodes (15–20h/day)

India-Specific Clinical Context

OSA: India's Hidden Epidemic

India has an estimated 50+ million people with OSA — one of the highest absolute burdens in the world. Risk factors prominent in India: central obesity, retrognathia (common in Asian populations, predisposing to airway collapse at lower BMI than Western populations), nasal septal deviation, and adenotonsillar hypertrophy in children. Many patients present to cardiologists or neurologists before OSA is identified as the underlying driver.

Narcolepsy Diagnostic Delay

The average diagnostic delay for narcolepsy in India is 10–15 years from symptom onset. Common misdiagnoses: depression (for hypersomnia and cataplexy misinterpreted as weakness from mood disorder); epilepsy (for cataplexy episodes or sleep paralysis); and malingering or laziness, particularly in school-age children whose academic performance drops.

RBD and Parkinson's Counselling

Isolated RBD predicts synucleinopathy in 80–90% of cases over 10–15 years. This creates a profound counselling obligation: patients deserve to know their prognosis honestly, to be enrolled in monitoring programmes, and to have access to neuroprotection clinical trials. At KIMS, every new RBD diagnosis prompts assessment for pre-motor Parkinson's features.

RLS and Iron Deficiency in India

Iron deficiency anaemia is highly prevalent in India, particularly in women of reproductive age, vegetarians, and patients with chronic kidney disease. It is the most common and most modifiable cause of secondary RLS. The target for RLS management is ferritin >75–100 mcg/L — significantly higher than the standard anaemia threshold of 12 mcg/L.

Conditions We Treat

01

Narcolepsy

Chronic neurological disorder caused by loss of orexin (hypocretin)-producing neurons. MSLT diagnosis and modern pharmacotherapy.

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02

Obstructive Sleep Apnoea (OSA)

Upper airway repeatedly collapses during sleep. CPAP — the most effective treatment for moderate-severe OSA.

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03

REM Sleep Behaviour Disorder (RBD)

Dream enactment from failure of REM atonia. Most powerful prodromal marker of Parkinson's and Lewy body dementia.

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04

Kleine-Levin Syndrome (KLS)

Rare recurrent hypersomnia in adolescents — episodes of 15–20h/day sleep with cognitive and behavioural changes.

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05

Restless Legs Syndrome (RLS)

Sensorimotor disorder with strong iron-deficiency link. Targeted ferritin optimisation and dopaminergic therapy.

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06

Non-24-Hour Sleep-Wake Disorder

Circadian rhythm disorder common in totally blind individuals. Tasimelteon and chronotherapy.

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07

Parasomnias

Abnormal behaviours, movements, or experiences arising from sleep. NREM parasomnias emerge from slow-wave (deep) sleep: sleepwalking (complex, coordinated nocturnal behaviour with full amnesia), sleep terrors (sudden arousal with screaming and intense autonomic activation but no dream recall), confusional arousals, and sleep-related eating disorder. REM parasomnias include nightmare disorder and recurrent isolated sleep paralysis; REM sleep behaviour disorder (RBD) is covered separately. Video-polysomnography distinguishes parasomnias from nocturnal frontal lobe epilepsy, which can appear identical clinically.

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The KIMS Sleep Programme Pillars

Gold-Standard Diagnostics

In-laboratory polysomnography (16+ channels: EEG, EMG, EOG, oxygen saturation, airflow, video), MSLT, MWT, and home sleep apnoea testing.

CPAP Therapy

Comprehensive CPAP initiation and titration for OSA — eliminates apnoeas and restores normal sleep architecture within 1–2 weeks.

Evidence-Based Pharmacotherapy

Modafinil, sodium oxybate, pitolisant, clonazepam, melatonin, tasimelteon — full spectrum of approved sleep-disorder therapies.

Synucleinopathy Surveillance

Long-term neurological monitoring of RBD patients for early Parkinson's and Lewy body dementia detection.

Expert Consultation

Our sleep medicine team reviews every complex case. Appointments: 040-44885000.

Why Choose KIMS Neuroscience?
  • In-laboratory polysomnography (16+ channels)

  • Dedicated MSLT for narcolepsy diagnosis

  • CPAP initiation, titration & long-term follow-up

  • RBD synucleinopathy surveillance programme

Sleep Diagnostics at KIMS
  • In-laboratory polysomnography (PSG)

  • Multiple Sleep Latency Test (MSLT)

  • Maintenance of Wakefulness Test (MWT)

  • Home sleep apnoea testing

  • Actigraphy

  • CPAP titration

  • Epworth Sleepiness Scale & validated questionnaires

International Patients
Dedicated support & travel coordinationneuroscience@kimshospitals.com

Sleep Disorders at a Glance

A comparative view of mechanism, key features, diagnostic approach, and primary treatment for all six conditions.

ConditionMechanismKey FeaturesDiagnosis at KIMSPrimary Treatment
NarcolepsyOrexin (hypocretin) deficiency from autoimmune destruction of hypothalamic neuronsExcessive daytime sleepiness, cataplexy (NT1), sleep paralysis, hypnagogic hallucinations, fragmented night sleepMSLT: mean sleep latency <8 min + ≥2 SOREMPs · CSF orexin <110 pg/mL (NT1) · HLA DQB1*06:02Modafinil/armodafinil · Sodium oxybate · Pitolisant · Venlafaxine (cataplexy)
Obstructive Sleep ApnoeaUpper airway collapse during sleep from anatomical and muscular factorsLoud snoring, witnessed apnoeas, unrefreshing sleep, morning headache, daytime sleepiness, nocturia · ↑ CVD and stroke riskPolysomnography: AHI ≥5 · Home sleep test for uncomplicated OSA · Epworth Sleepiness ScaleCPAP (gold standard) · Weight loss · Mandibular advancement device · Positional therapy · Surgery (selected)
REM Sleep Behaviour DisorderFailure of REM sleep atonia from brainstem (sublaterodorsal nucleus) dysfunction · Strong prodromal marker of synucleinopathyDream enactment during REM sleep — shouting, hitting, kicking, falling out of bed · Vivid, often violent dream contentPSG: REM sleep without atonia (RSWA) · Video-PSG for behaviour capture · Alpha-synuclein seeding assay (research)Clonazepam or melatonin · Bed safety modifications · Neuroprotection trials · Parkinson's monitoring
Kleine-Levin SyndromeUnknown; immune, genetic, and hypothalamic dysfunction proposed · MRI functional hypometabolism in thalamus during episodesRecurrent hypersomnia episodes (15–20h/day) lasting days–weeks, cognitive disturbance, derealization, hyperphagia, hypersexualityClinical diagnosis (ICSD-3 criteria) · EEG: generalised slowing during episodes · MRI brain (usually normal) · Exclude encephalitisLithium (reduces frequency/severity) · No proven acute treatment · Amantadine tried · Family and school counselling
Restless Legs SyndromeDopaminergic dysfunction + iron deficiency in the CNS · Genetic (BTBD9, MEIS1, MAP2K5) + secondary causesUrge to move legs at rest, worse evening/night, relieved by movement · Periodic limb movements in sleep (PLMS) on PSGClinical diagnosis (IRLSSG criteria — 5 essential features) · Serum ferritin (target >75–100 mcg/L) · PSG if PLMS assessment neededIron supplementation · Dopamine agonists: pramipexole, ropinirole · Alpha-2-delta ligands: gabapentin, pregabalin
Non-24-Hour Sleep-Wake DisorderFailure of circadian light entrainment · Most common in totally blind (no light input to SCN) · Rare sighted variantFree-running circadian rhythm producing daily progressive delay in sleep timing · Cyclical insomnia and daytime sleepinessActigraphy (2+ weeks) · Melatonin timing assay (DLMO) · Sleep diary · Confirm visual statusTasimelteon (Hetlioz) for blind individuals · Melatonin at fixed evening time · Light therapy in sighted N24
Parasomnias (NREM and REM)NREM parasomnias: incomplete arousal from slow-wave (N3) sleep with preserved motor activity · REM: nightmare disorder from abnormal REM processing; sleep paralysis from REM atonia persisting into wakefulnessNREM: Sleepwalking (complex behaviour, amnesia for event) · Sleep terrors (screaming, tachycardia, no dream recall) · Confusional arousals · Sleep-related eating disorder · REM: Nightmare disorder · Recurrent isolated sleep paralysisVideo-PSG (essential to distinguish from nocturnal frontal lobe epilepsy) · NREM parasomnias: Stage N3 arousal features on PSG · Seizure screen: LTM-EEG if seizure uncertain · Exclude OSA as a trigger for NREM parasomniasNREM: Sleep hygiene, safety precautions, scheduled awakenings · Clonazepam (NREM parasomnias and RBD) · Melatonin · Treat underlying OSA if present · Nightmare disorder: Image Rehearsal Therapy (IRT) · Prazosin for PTSD-related nightmares

Common Questions

Yes — loud snoring combined with unrefreshing sleep despite adequate time in bed is the most classic presentation of obstructive sleep apnoea. The snoring is the sound of the airway partially collapsing; the unrefreshing sleep reflects the dozens to hundreds of micro-arousals each night as the brain briefly wakes to restore airway muscle tone after each apnoea. A polysomnography or home sleep test at KIMS measures the apnoea-hypopnoea index (AHI) — the number of breathing interruptions per hour — and confirms the diagnosis. CPAP therapy eliminates the apnoeas, restores normal sleep architecture, and typically produces a dramatic improvement in daytime energy and functioning within 1–2 weeks. Call 040-44885000.

Narcolepsy typically begins in adolescence or young adulthood. The excessive daytime sleepiness of narcolepsy is qualitatively different from normal tiredness: it is sudden, irresistible sleep attacks that occur without warning in stimulating situations, followed by brief refreshing sleep and then recurrence within 1–2 hours. If your son also has brief episodes of muscle weakness triggered by laughter, surprise, or strong emotion (cataplexy — even if subtle, like a slight knee-buckle or head drop when laughing), narcolepsy with cataplexy (Type 1) is the most likely diagnosis. At KIMS, the Multiple Sleep Latency Test (MSLT) — a formal daytime nap study — confirms narcolepsy by documenting sleep-onset REM periods occurring abnormally quickly. Call 040-44885000.

What you are describing is REM sleep behaviour disorder (RBD). In RBD, the normal muscle paralysis of REM sleep fails, and the person physically acts out their dream content. This is dangerous: falling out of bed, punching or kicking a bed partner, and striking furniture during vigorous dream enactment have caused significant injuries. The neurological significance extends beyond the immediate safety risk: RBD is a prodromal marker of Parkinson's disease and Lewy body dementia in approximately 80–90% of cases over 10–15 years. At KIMS, RBD is diagnosed by polysomnography, bed safety modifications are recommended immediately, and a long-term neurological monitoring programme is initiated. Call 040-44885000.

Restless legs syndrome (RLS) and nocturnal leg cramps are distinct and often confused. RLS: an uncomfortable urge to move the legs (crawling, tingling, or creeping sensations), occurring at rest (particularly when sitting or lying down), worse in the evening and night, and partially relieved by movement. The urge to move is the defining feature — not pain. Nocturnal leg cramps: sudden, involuntary, painful muscle contractions (usually calf muscles) lasting seconds to minutes, resolved by stretching. RLS also differs from peripheral neuropathy (constant, positional-independent symptoms) and peripheral vascular disease (pain on walking, not at rest). At KIMS, RLS is diagnosed clinically using the four IRLSSG criteria and serum ferritin is measured as the first investigation. Call 040-44885000.

Simple snoring is noisy breathing during sleep without breathing interruptions, oxygen desaturation, or arousals. OSA is repeated complete or partial airway collapse causing pauses in breathing, drops in oxygen saturation, and micro-arousals throughout the night. The clinical clue is unrefreshing sleep despite adequate hours plus witnessed apnoeas or daytime sleepiness. A polysomnography at KIMS distinguishes the two: an apnoea-hypopnoea index of 5 or more confirms OSA.

Yes — direct sleep-clinic appointments are accepted. Outpatient: 040-44885000 (Mon–Sat). If you have prior sleep studies, bring the AHI report and the original polysomnography traces. CPAP machines from any manufacturer can be reviewed and re-titrated at the KIMS sleep laboratory.

Initial consultation is 30–60 minutes. A full in-laboratory polysomnography is an overnight stay in the sleep laboratory. The MSLT (for suspected narcolepsy) is a daytime study following the overnight polysomnography. Home sleep apnoea testing for uncomplicated OSA is done over a single night at home. Reports are typically available within 1–2 weeks.

Yes. Obstructive sleep apnoea is the most common secondary cause of treatment-resistant hypertension, and increases stroke risk 2–3 times and atrial fibrillation risk 3–4 times. CPAP therapy reduces blood pressure and cardiovascular risk. Any patient with unexplained hypertension and snoring should be tested for OSA at KIMS.

RBD occurs in the second half of the night from REM (dream) sleep; behaviour is purposeful, mimicking dream content (punching, kicking a real attacker). Sleepwalking occurs in the first half of the night from deep NREM sleep; behaviour is confused and non-purposeful. EEG during the episode confirms which stage. The neurological significance is completely different: RBD predicts Parkinson's disease in 80–90% of cases; sleepwalking does not.

Sleep is Not Optional

The brain repairs, the body restores, and memory consolidates during sleep. Sleep disorders at every level are diagnosable and treatable with evidence-based interventions that change lives.

040-44885000

International enquiries: neuroscience@kimshospitals.com