EMERGENCY:Witnessed apnoeas in known OSA · Dream enactment causing injury · Cataplexy causing falls in untreated narcolepsy —call040-46324365immediately — 24 hours, 7 days— 24/7
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.
7 Sleep Disorders
Polysomnography & MSLT
040-46324365
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.
| Fact | Details |
|---|---|
| Conditions covered | Narcolepsy · OSA · RBD · Kleine-Levin Syndrome · RLS · Non-24-Hour Sleep-Wake Disorder · Parasomnias |
| OSA burden in India | 50+ 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 delay | Average 10–15 years from symptom onset in India · Common misdiagnoses: depression (hypersomnia), epilepsy (cataplexy or sleep paralysis), laziness or malingering (declining school performance) |
| RBD prognosis | Isolated 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 iron | Iron-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 OSA | Gold-standard treatment · Eliminates apnoeas and restores sleep architecture within 1–2 weeks · KIMS provides full CPAP initiation, titration, and follow-up |
| Contact | 040-44885000 (outpatient) · 040-46324365 (emergency) · No referral required |
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.
• 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 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.
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.
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.
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.
Chronic neurological disorder caused by loss of orexin (hypocretin)-producing neurons. MSLT diagnosis and modern pharmacotherapy.
View Details →Upper airway repeatedly collapses during sleep. CPAP — the most effective treatment for moderate-severe OSA.
View Details →Dream enactment from failure of REM atonia. Most powerful prodromal marker of Parkinson's and Lewy body dementia.
View Details →Rare recurrent hypersomnia in adolescents — episodes of 15–20h/day sleep with cognitive and behavioural changes.
View Details →Sensorimotor disorder with strong iron-deficiency link. Targeted ferritin optimisation and dopaminergic therapy.
View Details →Circadian rhythm disorder common in totally blind individuals. Tasimelteon and chronotherapy.
View Details →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.
View Details →In-laboratory polysomnography (16+ channels: EEG, EMG, EOG, oxygen saturation, airflow, video), MSLT, MWT, and home sleep apnoea testing.
Comprehensive CPAP initiation and titration for OSA — eliminates apnoeas and restores normal sleep architecture within 1–2 weeks.
Modafinil, sodium oxybate, pitolisant, clonazepam, melatonin, tasimelteon — full spectrum of approved sleep-disorder therapies.
Long-term neurological monitoring of RBD patients for early Parkinson's and Lewy body dementia detection.
Our sleep medicine team reviews every complex case. Appointments: 040-44885000.
In-laboratory polysomnography (16+ channels)
Dedicated MSLT for narcolepsy diagnosis
CPAP initiation, titration & long-term follow-up
RBD synucleinopathy surveillance programme
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
A comparative view of mechanism, key features, diagnostic approach, and primary treatment for all six conditions.
| Condition | Mechanism | Key Features | Diagnosis at KIMS | Primary Treatment |
|---|---|---|---|---|
| Narcolepsy | Orexin (hypocretin) deficiency from autoimmune destruction of hypothalamic neurons | Excessive daytime sleepiness, cataplexy (NT1), sleep paralysis, hypnagogic hallucinations, fragmented night sleep | MSLT: mean sleep latency <8 min + ≥2 SOREMPs · CSF orexin <110 pg/mL (NT1) · HLA DQB1*06:02 | Modafinil/armodafinil · Sodium oxybate · Pitolisant · Venlafaxine (cataplexy) |
| Obstructive Sleep Apnoea | Upper airway collapse during sleep from anatomical and muscular factors | Loud snoring, witnessed apnoeas, unrefreshing sleep, morning headache, daytime sleepiness, nocturia · ↑ CVD and stroke risk | Polysomnography: AHI ≥5 · Home sleep test for uncomplicated OSA · Epworth Sleepiness Scale | CPAP (gold standard) · Weight loss · Mandibular advancement device · Positional therapy · Surgery (selected) |
| REM Sleep Behaviour Disorder | Failure of REM sleep atonia from brainstem (sublaterodorsal nucleus) dysfunction · Strong prodromal marker of synucleinopathy | Dream enactment during REM sleep — shouting, hitting, kicking, falling out of bed · Vivid, often violent dream content | PSG: 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 Syndrome | Unknown; immune, genetic, and hypothalamic dysfunction proposed · MRI functional hypometabolism in thalamus during episodes | Recurrent hypersomnia episodes (15–20h/day) lasting days–weeks, cognitive disturbance, derealization, hyperphagia, hypersexuality | Clinical diagnosis (ICSD-3 criteria) · EEG: generalised slowing during episodes · MRI brain (usually normal) · Exclude encephalitis | Lithium (reduces frequency/severity) · No proven acute treatment · Amantadine tried · Family and school counselling |
| Restless Legs Syndrome | Dopaminergic dysfunction + iron deficiency in the CNS · Genetic (BTBD9, MEIS1, MAP2K5) + secondary causes | Urge to move legs at rest, worse evening/night, relieved by movement · Periodic limb movements in sleep (PLMS) on PSG | Clinical diagnosis (IRLSSG criteria — 5 essential features) · Serum ferritin (target >75–100 mcg/L) · PSG if PLMS assessment needed | Iron supplementation · Dopamine agonists: pramipexole, ropinirole · Alpha-2-delta ligands: gabapentin, pregabalin |
| Non-24-Hour Sleep-Wake Disorder | Failure of circadian light entrainment · Most common in totally blind (no light input to SCN) · Rare sighted variant | Free-running circadian rhythm producing daily progressive delay in sleep timing · Cyclical insomnia and daytime sleepiness | Actigraphy (2+ weeks) · Melatonin timing assay (DLMO) · Sleep diary · Confirm visual status | Tasimelteon (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 wakefulness | NREM: 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 paralysis | Video-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 parasomnias | NREM: 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 |
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.
International enquiries: neuroscience@kimshospitals.com