Where things stand now
The essentials for a clinician meeting him for the first time.
| Medicine | Dose & timing | Status | Role |
|---|---|---|---|
| Quetiapine | 100 mg · twice daily | Taking | Low, maintenance-level antipsychotic; relatively Parkinson's-safe (corrected 9 Jul — twice daily, not once) |
| Levodopa / Carbidopa (LCD) | 110 mg · twice daily | Taking | Dopamine replacement for Parkinsonism. Confirmed 11 Jul: twice daily, not the three-times-daily (1-1-1) schedule the neurologist originally prescribed — flagged to the prescriber, not changed independently; may leave an uncovered "off" interval |
| Pimavanserin | 34 mg · night | Taking | A newer antipsychotic (5-HT2A inverse agonist) that calms psychosis without blocking dopamine — so it doesn't worsen the stiffness/slowness. Added when aripiprazole was stopped (30 Jun). Independently recommended by two psychiatrists (Dr. Virinchi Sharma and Dr. Jyothirmayi, Manaha Clinic) |
| Vortioxetine | 5 mg · night | Not taking | Prescribed for pain (serotonergic modulation) but not actually being taken |
| Aripiprazole | was 5 mg | Stopped | The high-D2-occupancy "clamp"; discontinued 30 Jun 2026. Briefly restarted for a couple of days in early-mid Jul 2026, then stopped again — not continuing |
Background / standing medicines: Vitamin B12 injection (Meaxon) weekly · Vitamin D3 60 K weekly · Carniglo-M (L-carnitine + B12). Gabapentin 300 mg at night is not currently being taken (confirmed 11 Jul) — earlier sessions in this log spent considerable effort on optimising it for neuropathic/movement-evoked pain; since it has lapsed, that pain coverage is currently absent and worth raising with the prescriber. The 30 June change moved the regimen decisively toward less dopamine blockade while keeping antipsychotic cover — the direction earlier analysis recommended.
The pivotal observation: two tracks, mostly overlapping
When Nanna is at his worst, immobility, pain, delusion and hallucinations appear together — which first looked like one single problem. But a key refinement (10 Jul): the immobility can occur on its own, with no psychosis at all — and that is his commonest stuck state. So it is better read as a baseline movement problem with an on-and-off psychosis layered on top.
Reframe · 10 Jul 2026 — what actually stops him getting up
A close clarification of the "stuck" state, corrected in stages. The reliable part is what happens; the why is genuinely still open. Earlier drafts of this page called the immobility "catatonic" and made a lorazepam challenge the headline test — that is now retracted. The barrier is pain, not a painless motor block, and lorazepam does not treat pain.
What's solid
- ·He wants to move and tries — volition and speech are intact.
- ·The barrier is pain below the buttocks. Until it's solved he can't get up — it's the preventing reason.
- ·The pain is triggered by moving — any attempt to change position. He can lie still without it.
- ·When it's bad he cannot even sit — so it's not simply relieved by a flexed/sitting posture.
- ·He can't push through a bad day; the pain doesn't ease with effort. Good days arrive all of a sudden.
What it rules out
- ✕Catatonia — he wants to move; pain is the gate, not absent drive.
- ✕Painless freezing — pain, not initiation, is the barrier.
- ✕"Walking claudication" from stenosis — he walks hundreds of metres fine on good days.
- ✕Simple positional stenosis — sitting doesn't reliably relieve it (can't even sit when bad).
- ✕A fixed lesion acting alone — disc/spine/hip anatomy doesn't switch on and off overnight.
The unexplained key clue: something is switching the pain fully on and off, abruptly, day to day. A fixed mechanical problem can't do that alone — so either a nerve root is intermittently inflamed, or the pain is being gated by a fluctuating neurological/neuropsychiatric state, or there's a hip/pelvic source. None confirmed.
Priority next step: an in-person exam caught during a bad episode — does passively moving his leg reproduce the pain? Hip vs nerve-root vs spine? That will settle more in ten minutes than further reasoning from description. Gabapentin, discussed at length here as under-dosed, has since lapsed entirely (confirmed 11 Jul not being taken) — restarting and optimising it is on the table for the pain; hold the L3–L4 epidural steroid injection as an option if an exam supports a nerve-root source.
Stuck phase
- Immobile — cannot rise from lying or sitting; pain below the buttocks on any attempt to move
- Pain is movement-evoked — the 10 Jul clarification indicates he can lie still without it; it is triggered by trying to change position (this supersedes an earlier "pain at rest too" note — the point is unsettled and worth confirming)
- "Electric fields" delusion — believes someone is sending fields to cause the pain (a somatic passivity delusion — a false belief that an outside force is controlling his body)
- Hallucinations — both visual and auditory, present in this phase
- Shouts at his persecutors; afterwards the "field" and pain ease
Walking phase
- Walks fully & normally — to the supermarket, sustained for hours
- No rest pain — pain is entirely absent
- No delusion — the electric-fields belief is gone
- No hallucinations — visual and auditory both absent
- His own words: "when the connection is cut, I have no problems"
The earlier reading: whenever pain appeared it seemed to track the delusion — he attributes it to the electric fields, it eases when he shouts at the hallucinated attacker, and it vanishes on well days — which looked like part of the psychotic layer rather than tissue pain, making orthopaedic work-up low-yield.
The 10 Jul reframe qualifies this. The pain that actually prevents him getting up is movement-evoked, located below the buttocks, and blocks him even when there is no psychosis present. That is behaving like a physical/neurological pain gate, not purely a psychotic symptom — so a structural / neurological cause is back on the table for that pain, and an in-person exam is warranted. The two may be different things (a delusion-linked pain during florid phases vs. a movement-evoked barrier pain), or the "tracks the delusion" claim was over-stated. This is genuinely unresolved and is exactly what a hands-on exam during a bad episode should clarify.
Refinement · 10 Jul 2026 — it's not all one switch
A closer look shows the immobility and the psychosis are separable. There are really three states, and the most common "stuck" state has no psychosis in it at all:
| State | Movement | Psychosis | Pain | How often |
|---|---|---|---|---|
| Stuck, no psychosis | Stuck | None | Movement-evoked pain below the buttocks gates his rising (per 10 Jul reframe) | Most common stuck state |
| Full bad phase | Stuck | Electric-fields delusion + hallucinations | Present | Less frequent |
| Good phase | Walks normally | None | None | ~1 day in 5–6 |
Two consequences. (1) The "stuck" state is not just a symptom of the psychosis — it has its own driver. The 10 Jul reframe identifies that driver as movement-evoked pain below the buttocks (not a painless catatonic freeze, as an earlier draft supposed) — so a stronger antipsychotic alone would not be expected to release the stuck state, and the priority is an in-person exam of that pain during a bad episode, not a lorazepam challenge. (2) During florid phases the pain also gets attributed to the electric fields — so there may be a delusion-linked pain and a physical movement-evoked barrier pain; telling them apart is an open question.
A witnessed episode · 10 Jul 2026
During a stuck-phase pain episode, Nanna said the pain was coming as "waves through the air cooler", and was shouting and swearing to drive off the imaginary people causing it — now believing his wife was helping to instigate them. Telling him she was simply in the bathroom, and then moving the air cooler out of the room, calmed him down and the pain settled.
Two things stand out. The belief has attached to a specific object (the cooler as a "wave emitter") and now names a family member as a co-conspirator — both signs of active, not-fully-controlled psychosis. And once again the pain eased through calming and removing the object, not a painkiller — more evidence it tracks the belief, not tissue damage. Gentle reassurance plus removing the fixated-on object de-escalated him without confrontation — a useful caregiving approach, though whether to keep accommodating the delusion this way is worth raising with the psychiatrist.
How the diagnosis converged — and then split in two
The working picture arrived by ruling things out — the spine and soft-tissue leads were investigated and demoted, and a neuropsychiatric model emerged for the psychosis. But the 10 Jul reframe then separated the immobility back out: its barrier is a movement-evoked pain whose cause is not settled, so the physical/neurological question is reopened for that track.
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Mar 2026 · crisisCouldn't get up for 2 daysFollowed a 15-month gap off all medicines. Resolved with levodopa + B12 — a physical, dopamine-deficiency crisis, before antipsychotics were restarted.
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Apr–May 2026 · spine leadLumbar MRI → stenosis at L3–L4Real degenerative findings. But 3 of 4 specialists (incl. the treating neurologist and a UK MSK radiologist) read them as background age-related change — not enough to explain being bedbound while also walking to the shops other days.
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May 2026 · soft-tissue leadA "sitting-bone" inflammation ideaIschiogluteal bursitis — inflammation where the body meets a chair — fit the "can't rise" pattern for a while. Then broken by three findings: recovery was always preceded by a night of talking (a warning sign a pure muscle problem can't explain), reducing crawling didn't help, and pressing the sore spot didn't reproduce the pain.
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17 May 2026 · the pivotA medicine-driven brain cycleEverything switching on and off together, fully clearing on good days, in a brain made over-sensitive by 20+ years of antipsychotics — a "periodic catatonia" type picture. (iatrogenic dopaminergic oscillation)
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Jul 2026 · direct confirmationThe delusion + hallucinations surfacedThe electric-fields somatic delusion and the visual + auditory hallucinations — present only in stuck phases — are the first directly observed active psychotic symptoms, corroborating the model rather than inferring it.
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9 Jul 2026 · confirmedZero pain on walking days — no exceptionDuring walking (good) days he has no pain at all — the pain is 100% confined to stuck phases, same as the delusion. (An earlier note here said "rest pain" occurs in stuck phases; the 10 Jul clarification revises that to movement-evoked pain — he can lie still without it. The point is unsettled and worth confirming directly.)
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10 Jul 2026 · the splitThe immobility is pain-gated — physical question reopenedThe thing that actually stops him rising is movement-evoked pain below the buttocks, present even without psychosis. This is not catatonia (he wants to move), not painless freezing, not walking-claudication (he walks fine on good days), and not simple positional stenosis (can't even sit when bad). But the abrupt, complete day-to-day switching of the pain can't come from a fixed lesion alone. Cause unresolved → an in-person exam during a bad episode is the priority, and the lorazepam challenge is dropped for the immobility.
The mechanism, in short — for the psychosis track
This explains the psychosis overlay (delusion, hallucinations) and its on/off timing. It does not by itself explain the movement-evoked pain that gates his rising — that is the separate, still-unexplained track (see the 10 Jul reframe in section 2).
Two decades of antipsychotics blunted his brain's dopamine signals, so the system became over-sensitive to compensate. On top of that, aripiprazole acted like a "clamp" holding the dopamine receptors shut — one the over-sensitive brain kept straining against. Every so often the brain's own surge breaks through the clamp (seen as the night-talking), and he has a good day. (Clinically: D2 supersensitisation with an iatrogenic dopaminergic oscillation.)
Why extra levodopa doesn't rescue a stuck phase: the bottleneck is receptor occupancy by the antipsychotic, not a shortage of dopamine — so more levodopa can't push past an already-occupied receptor. Stopping aripiprazole (done 30 Jun) directly tests this.
| Voice | Verdict |
|---|---|
| Dr. Neehar (treating neurologist) | Disability disproportionate to pathology — primarily psychiatric; see a psychiatrist |
| Dr. Sudhakar (UK MSK radiologist) | Mild, age-appropriate changes; not surgical |
| Original MRI report | Findings listed; "correlate clinically" (hedged) |
| Rakesh (ortho surgeon, informal) | Initially surgery; later revised — "if he can walk to the supermarket, it's not primarily the spine" |
Other possibilities still on the table
Two questions now, not one. For the psychosis overlay, the cyclical drug-driven model leads (below). For the immobility, the 10 Jul reframe leaves the cause of the movement-evoked pain open — so several of these entries (Lewy body, levodopa off-period, and a physical nerve-root/spine source) are live candidates for the motor/pain track specifically. What still narrows the list is that the whole picture fluctuates abruptly and completely day to day — few conditions do that.
Tier 1 · best fits for the all-or-nothing cycle
Tier 2 · physiological contributors that could ride on the cycle
Silent recurring triggers of confusion (delirium) — a hidden urine infection, constipation, dehydration swings, or night-time drops in oxygen from sleep apnoea (which would also fit the night-talking). Cheap to screen: urine test during a bad phase, overnight oxygen check.
Non-epileptic brain "arrest" episodes — a form of epilepsy that causes behavioural freezing rather than convulsions; the March EEG can miss it. Test: repeat EEG during a stuck phase.
B12-deficiency brain/nerve disease — 15 months unsupplemented can cause psychosis and worse neuropathy. The earlier B12 result was falsely high. Test: MMA + homocysteine (the true B12 status).
Swinging body chemistry — thyroid, sodium, calcium, kidney values checked during a bad phase vs a good one. A value that repeatedly swings is one of the few things that genuinely produces on/off days.
Tier 3 · rare, but each a single cheap rule-out
Autoimmune encephalitis — the one rare disease that naturally produces psychosis + catatonia + movement problems + pain together and fluctuates; usually comes on over weeks (the March crash qualifies). One blood panel. · Neurosyphilis / HIV — old-fashioned, cheap rule-outs for late-life psychosis, likely never tested. · Paraneoplastic syndrome (a hidden cancer driving the nerve + brain picture) — only if the above come back clean. · Normal-pressure hydrocephalus — gait + memory + urinary, but it doesn't cycle; low probability.
1. In-person exam during a bad episode — the priority for the immobility: does passively moving his leg reproduce the pain? Hip vs nerve-root vs spine? Settles more than any remote reasoning. 2. Levodopa-timing vs stuck-phase diary — free; tests the "off-state" idea and whether good days track a dose. 3. DAT-SPECT — drug-induced vs Lewy-body/degenerative Parkinsonism; decides whether the levodopa lever or the antipsychotic lever is the main one. 4. One "bad-phase" blood/urine panel — sweeps Tier 2 in a single draw. 5. Autoimmune / syphilis / HIV serology — sweeps Tier 3 if 1–4 are unrevealing.
On the lorazepam challenge: it has dropped down the list. It was premised on the immobility being catatonic; the 10 Jul reframe (pain is the gate, volition intact) makes that unlikely, and lorazepam doesn't treat pain — plus his falls/sedation profile (Beers-listed; neuropathy and balance impairment) argues against it. It becomes relevant again only if an in-person exam actually turns up catatonic signs.
Bottom line: the immobility and the psychosis are now two questions. The exam + levodopa-timing diary address the movement-evoked pain; the pimavanserin trial and antipsychotic strategy address the psychosis. Both are low-cost and can run in parallel over the coming weeks.
Two differentials, reconciled — 11 July
A second, independent differential (11 Jul) was built on the corrected description of the problem. It does not replace the tiered list above — it re-anchors it. Because the two were built on different pictures of what is actually happening, they disagree; this section reconciles them and states which options to act on.
Why the two disagree — different phenomenology
10 Jul tiered list was built on the earlier framing: "genuinely stuck ~80% of the time; immobility + rest pain + psychosis all switch on and off together." Treating the cyclicity as the master clue, it ranked periodic catatonia, dopamine oscillation, and Lewy body disease at the top, and named the lorazepam challenge as the headline test.
11 Jul differential was built on the corrected picture: this is not painless immobility but movement/transition-evoked pain below the buttocks, with volition intact and no rest pain, fully remitting on good days when he walks for hours. That correction removes the foundation of the 10 Jul top tier — catatonia falls to low probability and the lorazepam challenge loses its rationale.
The 11 July differential — what a diagnosis must explain, and how to verify it
| Possibility | Why it stays relevant | Best way to verify |
|---|---|---|
| Dynamic lumbar nerve-root pain — L3–L4 stenosis / spondylolisthesis | MRI confirms L3–L4 recess stenosis, root compression, and a Grade I slip. May contribute even though the pattern isn't classic claudication. | In-person exam during a bad day: strength, reflexes, sensory map, straight-leg-raise/slump, lumbar movement; standing flexion-extension X-rays. Targeted root block / epidural only if exam and imaging correlate. |
| Hip / pelvic / deep-gluteal / proximal-hamstring pathology | Most painful during transfers — and easily missed by a lumbar MRI. Fits "can't transfer but walks fine once up." | Passive hip range, FABER/FADIR, resisted hamstring, focal palpation; pelvis/hip X-ray first, then pelvic MRI or ultrasound if indicated. |
| Sacral / pelvic insufficiency fracture (the "don't miss") | Age + the vitamin-D-deficient gap + buttock-region pain. Can occur with no remembered fall and will not show on lumbar imaging. | Pelvis/hip X-ray; if suspicion persists despite a negative X-ray, pelvic MRI or CT. |
| Peripheral / nutritional neuropathy | Objectively confirmed and progressive on prior nerve studies; worsens pain, balance, and recovery — though it can't explain complete good-day normality by itself. | Repeat EMG/NCS; test vibration, pinprick, proprioception, ankle reflexes; review HbA1c, CBC, renal, folate, thyroid, and clinician-interpreted B12/MMA/homocysteine. |
| Proximal muscle disease / osteomalacia / metabolic myopathy | Painful proximal weakness impairs rising, especially after nutritional deficiency or with medication/metabolic contributors. | CK, vitamin D, calcium, phosphate, alkaline phosphatase, PTH, ESR/CRP, CBC, renal/liver, thyroid; review statins and other myotoxic drugs. |
| Levodopa off-state, rigidity, or dystonic pain | Levodopa is currently taken twice daily rather than the prescribed three times, leaving possible uncovered intervals that may amplify a separate pain generator. | 2–3 week diary of dose time, meal time, and pain/transfer ability just before and at 30/60/120 min after each dose; neurologist review in OFF and ON states. Do not alter doses without the prescriber. |
| Medication adverse effects / absorption / timing | Antipsychotic changes, levodopa–meal timing, dehydration, constipation, and poor sleep all change motor reserve and severity. | Full medication reconciliation from the actual strips and schedules; correlate symptoms prospectively with each change. |
| Functional / nociplastic pain modulation | The abrupt all-or-none switching raises it — but it must not be inferred from psychiatric history or non-specific imaging. | Neurologist / physiotherapist / pain specialist assessment for positive functional signs and a graded rehab plan. Not a diagnosis of exclusion. |
| Catatonia | Lower probability now — episodes are pain-limited with intact effort and volition — but history alone can't fully exclude it. | Formal bedside assessment during an episode for posturing, negativism, mutism, echophenomena. No home lorazepam challenge. |
| Episodic metabolic / seizure / delirium trigger | Low probability, but worth pursuing if episodes include altered awareness, stereotyped spells, confusion, fever, dehydration, constipation, or urinary symptoms. | During a bad phase: urinalysis, glucose, sodium, calcium, renal/liver, thyroid; EEG during an event only if seizure/altered-awareness features are present. |
| Underlying degenerative Parkinsonism / Lewy-body disease | Consider if parkinsonism, cognition, or visual hallucinations persist independently of medication changes and psychotic episodes. | Movement-disorder neurologist assessment; DAT-SPECT only if needed to separate drug-induced from degenerative parkinsonism. |
The two differentials fit together. The 11 Jul list identifies the proximate pain generator (most likely hip / pelvic / gluteal or dynamic nerve-root, with a sacral insufficiency fracture as the must-exclude). The 10 Jul list still contributes the one thing the table doesn't fully resolve — the abrupt, complete day-to-day switching, best explained by a fluctuating state gating the pain on and off (levodopa off-state / dystonic cycling), which is the cheapest, zero-risk thing to test.
Priority order: 1. In-person exam during a bad episode (hip vs root vs spine). 2. Pelvis/hip X-ray — then pelvic MRI if suspicion persists — to exclude a sacral insufficiency fracture the lumbar MRI can't see. 3. Focused labs: CK, vitamin D, Ca/PO₄, ALP, PTH; MMA + homocysteine (the >2000 B12 was post-injection and uninterpretable); thyroid, renal. 4. Levodopa-timing diary — free; tests the off-state contribution. 5. Drop the lorazepam challenge as a near-term step.
The single most useful reframing across both documents: stop treating this as one "stuck" syndrome. Separate the movement-evoked pain (peripheral / mechanical — needs an exam and a pelvis X-ray) from the psychotic overlay (a separate track). That separation, plus the sacral-fracture and hip/gluteal additions, is where the 11 Jul differential improves on the earlier tiered list.
First hands-on exam during a stuck day — 11 July
Every entry above has called for an in-person exam during a bad episode. Today was a confirmed stuck day, and Dr. Karthik — a paediatrician, AIIMS-trained, a family friend visiting for the afternoon — examined him close-up at home. It is the first hands-on look captured mid-episode, though not a formal specialist exam.
Reproducibility alone doesn't discriminate — it's consistent with two different explanations that predict the identical result:
FND-supportive reading: an alternate, less-automatic motor strategy (or external facilitation) unlocking a blocked pathway is a recognized positive sign of functional neurological disorder (cf. functional gait improving with backward walking or dancing).
Mechanical reading, equally strong: the prone push-up avoids the specific hip-flexion/loading angle a normal sit-up or stand-up transfer requires, and the assisted stand changes the load path through the hips/spine. A load-specific pain generator — hip, nerve root, or a sacral/pelvic source — predicts exactly the same reliable relief from exactly this maneuver.
What would actually discriminate (not yet tested): pain reproduced by passive movement of the hip/leg and focal tenderness on palpation over the sacrum/sit-bones/hip both point mechanical; a positive straight-leg-raise or FABER/FADIR points mechanical; relief generalising to any distraction or novel task, not just this one maneuver, points FND.
This is the first confirmed observation of the abrupt bad→good switch being triggered, rather than arriving spontaneously as on prior good days — new and useful regardless of cause. It does not rule out the physical differential (dynamic nerve-root pain, hip/pelvic/gluteal source, sacral insufficiency fracture, levodopa off-state/dystonic pain) — a mechanical, angle-specific pain generator predicts the same relief pattern seen today.
Not yet captured, worth getting next time: the time of his last levodopa dose relative to when the pain broke (tests the off-state theory at zero cost), whether relief came from the push-up itself vs. the assisted stand vs. simply elapsed time, and a short video of the sequence for a specialist to review later.
Action: log this as one voice on the differential, not a redirect of the workup. The in-person exam still needed is the same one called for since 10–11 Jul — passive hip/leg movement, straight-leg raise, focal palpation, and a pelvis/hip X-ray to exclude a sacral insufficiency fracture — ideally examining specifically for these signs during a bad phase.
The forward plan — two tracks
Since 10 Jul the plan splits: a psychosis path (adjust antipsychotic cover if pimavanserin proves too weak) and a separate immobility / pain path (get the movement-evoked pain examined and treated). Not a prescription — every step is a physician's decision.
To raise with Dr. Virinchi
- The electric-fields somatic delusion, and that pain / immobility / delusion cycle together
- That walking days are completely symptom-free
- That both visual and auditory hallucinations are present — raise levodopa as a possible contributor
- Whether current cover (pimavanserin + low quetiapine) is enough given florid symptoms in stuck phases
- That the immobility is gated by movement-evoked pain below the buttocks — arrange an in-person exam during a bad episode (hip vs nerve-root vs spine)
- A baseline ECG (pimavanserin can prolong QT)
- Decide whether to start or formally drop vortioxetine; confirm the LCD schedule
Reading the 4–6 week pimavanserin trial
Psychosis ↓ + walking returns → the psychosis was driving most of it; may need no escalation.
Psychosis ↓ but still stuck → confirms the immobility is a separate track → pursue the movement-evoked pain: in-person exam, not a lorazepam challenge.
No change in psychosis → pimavanserin too weak → escalate up the ladder.
Track A · Psychosis — escalation ladder if pimavanserin proves too weak
Uptitrate quetiapine
Lowest-friction antipsychotic step — already on it, relatively Parkinson's-safe, no new drug or monitoring. Watch sedation / falls; only moderate potency.
Clozapine
The one strong antipsychotic that controls psychosis without worsening movement — but needs regular blood monitoring and carries fall/sedation risk. (Interacts with benzodiazepines — additive CNS/respiratory depression — relevant only if a benzo is ever added.) Specialist decision.
Add valproate
If the defining problem is the periodicity of the psychosis, valproate targets the cycle directly, with no dopamine blockade — an adjunct, not a standalone antipsychotic.
ECT — for refractory cases
Highly effective and specifically indicated for severe psychosis (and for catatonia, should it ever be confirmed); in a frail elderly patient often safer than stacking sedating drugs. Reserved, but a genuine option.
Track B · Immobility / pain — get the movement-evoked pain examined and treated
In-person exam during a bad episode — the priority
The barrier is movement-evoked pain below the buttocks. A clinician examining him while he is stuck — passive leg movement, straight-leg-raise, localising hip vs nerve-root vs spine — will settle the cause faster than anything else. This is the single most useful next step for the immobility.
Restart and optimise gabapentin for the pain
Confirmed 11 Jul: gabapentin is not currently being taken — the 300 mg at night that earlier sessions flagged as under-dosed has since lapsed entirely, leaving no pharmacological cover for a neuropathic/nerve-root contributor. Restarting and then titrating up (there is substantial headroom before anything Beers-listed is needed) is low-risk and addresses that component directly — a prescriber decision.
L3–L4 epidural steroid injection — if the exam supports a nerve-root source
Both diagnostic and therapeutic for radicular pain. Held as conditional: pursue it only if the in-person exam points to the nerve root, since it won't address the abrupt on/off fluctuation.
Levodopa-timing diary alongside
Free. Log dose times against the sudden switches and whatever modifies the pain — tests whether an "off-state" component contributes, and whether DAT-SPECT (drug-induced vs degenerative Parkinsonism) is warranted.
Earlier drafts made this the headline test and the first escalation, on the assumption the immobility was catatonic. That assumption is now doubted: the barrier is pain with volition intact, and lorazepam does not treat pain. It also carries real risk here (Beers-listed; boxed warning if combined with a gabapentinoid — relevant again if gabapentin is restarted; falls risk from his neuropathy and balance impairment). It returns to the table only if an in-person exam actually turns up catatonic signs.
Avoid high-potency, strong D2-blocking antipsychotics — haloperidol, higher-dose risperidone or olanzapine. In someone with drug-induced Parkinsonism these worsen the stiffness/slowness (the 20-year trap that started all of this) and, in a frail elderly patient, risk triggering a rare, dangerous reaction (neuroleptic malignant syndrome / malignant catatonia). Flag this to any new doctor who, seeing severe psychosis, might reach for a strong older antipsychotic.
Reference
Supporting detail — history, tests, medication trail, and the care team.
Diagnoses in full
- Schizophrenia — long-standing (20+ years), well-controlled for most of that time on antipsychotic medicines (quetiapine / flupenthixol). Right now the symptoms (delusions, hallucinations) are active during the stuck phases.
- Drug-induced Parkinsonism — stiffness and slowness caused by those same long-term antipsychotics; it improves with levodopa.
- Nutritional nerve damage in both legs (peripheral neuropathy) — confirmed by nerve tests in Nov 2022 and worse by Dec 2024. Not from diabetes (blood sugar is normal); linked to vitamin deficiency.
- Cyclical psychosis — the current best explanation for the on/off delusion and hallucinations (see sections 2–3). Note (10 Jul): the immobility is now read as a separate, pain-gated problem rather than folded into this — its cause is still being worked out.
Other findings noted along the way: poor balance (Romberg's positive), some involuntary body-function irregularity (autonomic dysfunction), and one slightly low thyroid value (low T3). A blood-pressure reading of 145/102 (high) appears on prescriptions and was never acted on — but family says some readings were copied over from a template, so it needs a fresh, real measurement. No day-to-day memory loss seen at home.
Timeline of crises & prescription changes
Dec 2024 → Mar 2026 — he was off all medicines for about 15 months (levodopa, B12, vitamin D, nerve medicines, and antipsychotics). Telling detail: he went those 15 months with no antipsychotic and did not have a psychiatric breakdown.
18 Mar 2026 — crisis — couldn't get up for 2 days; levodopa + a B12 injection got him moving again. Video consult with Dr. Neeraja Alluri.
25 Mar 2026 — put on three antipsychotics at once (olanzapine + quetiapine + risperidone) — too much, and it drove the next crisis.
30–31 Mar 2026 — immobile again from too much dopamine blockade; the family stopped risperidone and he walked within 9 hours. Care moved back to Dr. Neehar, who simplified to a single antipsychotic (aripiprazole 5 mg) plus gabapentin and B12.
Apr–May 2026 — discovered his levodopa was being given wrong (twice a day, after food, instead of three times before food) and corrected it; the spine and muscle leads were investigated and set aside; care was briefly remote-only with Dr. Sudhakar (UK). By 11 Jul the schedule had reverted to twice daily — flagged to the prescriber, not yet resolved.
30 Jun 2026 — Dr. Virinchi Sharma (psychiatrist): stopped aripiprazole and added pimavanserin 34 mg; also prescribed vortioxetine (not being taken). This is the current shift toward less dopamine blockade. A second psychiatrist, Dr. Jyothirmayi (Manaha Clinic), independently recommended the same pimavanserin 34 mg.
Key investigations on record
Nerve tests (NCS / EMG) — Nov 2022 & Dec 2024: confirmed nerve damage in both legs, worse on the second test.
Brain wave test (EEG) — 25 Mar 2026: some abnormal electrical activity in the front/side of the brain, but not epilepsy; no seizure medicine needed.
Lower-back MRI scan — 6 May 2026: several age-related wear-and-tear changes, the main one a narrowing at the L3–L4 level pressing on nearby nerves. Most reviewers read these as normal-for-his-age background changes, not the cause of his disability.
Blood tests — the B12 result was falsely high because it was taken just after a B12 injection (a truer test is still pending); slightly low thyroid (T3); mild anaemia (low haemoglobin, 12.2).
Useful steps not yet done: an in-person exam of the movement-evoked pain during a bad episode (the priority for the immobility); a baseline heart-rhythm check (ECG, for the new medicine); a levodopa-timing diary; a repeat nerve test; and the fuller B12 tests. (The lorazepam challenge — prominent in earlier drafts — is now demoted; see section 5.)
Medication note (11 Jul): gabapentin — previously discussed at length in this record as under-dosed for neuropathic pain — is not currently being taken at all, and LCD has reverted to twice daily rather than the prescribed three times. Both are worth reconciling with the prescriber; neither has been changed independently by the family.
Care team
| Clinician | Role | Status |
|---|---|---|
| Dr. Virinchi Sharma | Psychiatrist — current prescriber (30 Jun 2026); prescribed pimavanserin 34 mg | Current |
| Dr. Jyothirmayi | Psychiatrist, Manaha Clinic — independent second opinion; also recommended pimavanserin 34 mg | Concurring |
| Dr. Neehar Potluri | Brain & nerve specialist (neurologist) — examined him in person over the longest period; view: "this is primarily psychiatric — see a psychiatrist" | Prior / key |
| Dr. Neeraja Alluri | Brain & nerve specialist (neurologist) — Mar 2026 | Discontinued |
| Dr. Sudhakar | UK bone/joint imaging specialist — reviewed scans remotely | Consultant |
| Rakesh | Orthopaedic surgeon — informal home review | Informal |
| Dr. Karthik | Paediatrician, AIIMS-trained — family friend; first hands-on exam captured during a bad episode (11 Jul), impression of conversion disorder | Informal |
A recurring recommendation in the record: find a trusted local doctor (a general physician or a specialist in elderly care) to be the on-the-ground prescriber who examines him and orders tests — several things (medicine changes, blood monitoring, any next step) can't be handled from a distance.
Contact & documents
Patient mobile: 7989480060 · Location: Miyapur, Hyderabad.
On file (not embedded here): Neehar Neuro Centre records (2022–2024), prescription photos, 25 Mar EEG, 6 May lumbar MRI report, Dr. Sudhakar exercise sheet, and the full running clinical log this overview summarises.