Friday, May 8, 2026

36M acute dissem encephalomyeloneuropathy seq Spastic Quadriparesis 1 year Telangana PaJR

 
08-05-2026

THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.

[3:24 pm, 08/05/2026] PPM 2: The image looks like the lower limbs also have LMN signs.
[3:29 pm, 08/05/2026] PPM 1: Yes
[3:36 pm, 08/05/2026] PPM 1: [08/05, 11:17]: Clinical examination of this 36M with spastic quadriparesis and spastic dysarthria after a febrile illness and episode of seizure one year back is suggestive of:
Slow effortful speech unable to articulate jointed words yuktaksharas such as "yudhishthir"
Power 3/5 in all limbs except left upper limb where it's 4/5
Tone increased in all four limbs with contractures
Deep tendon reflexes absent in left upper limb, bilateral knees
Planters equivocal 
@PaJR Health what's your input on the attached nerve conduction velocity findings here
[08/05, 12:51] Google Gemini manual prompt online as PaJR bot was unresponsive: Based on the Nerve Conduction Study (NCS) reports provided, there is evidence of a *diffuse, asymmetric sensorimotor polyneuropathy*, characterized by both axonal loss and demyelinating features.
However, the clinical picture you described—spastic quadriparesis, spastic dysarthria, and increased tone following a febrile illness/seizure—strongly points toward *Upper Motor Neuron (UMN)* involvement (likely a post-encephalitic or post-inflammatory sequel). The NCS findings indicate that there is an additional *Lower Motor Neuron (LMN)* or peripheral nerve component present, which may explain the absent reflexes you noted.
### Breakdown of NCS Findings
#### 1. Sensory Nerve Conduction (SNC)
* *Significant Abnormalities:* There is a marked reduction in Sensory Nerve Action Potential (SNAP) amplitudes across multiple nerves.
* *Left Median Nerve:* Amplitude is severely low ($5.3\ \mu V$).
* *Left Ulnar Nerve:* Amplitude is low ($2.8\ \mu V$) with a significantly slowed conduction velocity ($32.79\ m/s$).
* *Left Sural Nerve:* Very low amplitude ($2.5\ \mu V$).
* *Asymmetry:* Interestingly, the right-sided sensory nerves (Median and Sural) show relatively preserved or significantly higher amplitudes compared to the left, suggesting an asymmetric process.
#### 2. Motor Nerve Conduction (MNC)
* *Peroneal Nerves:* There is severe axonal loss. The *Left Peroneal* nerve shows a very low amplitude ($0.26\ mV$) at the ankle and *no response* at the knee. The Right Peroneal is also reduced ($0.86\ mV$).
* *Conduction Velocities:* Most motor conduction velocities are within the lower limit of normal or mildly slowed (e.g., Left Tibial at $41.48\ m/s$), which is often secondary to the loss of large-diameter fast-conducting axons.
#### 3. F-Wave Studies
* The Left Median F-wave shows a minimum latency of $23.00\ ms$, which is within normal limits. This suggests that despite the distal sensory/motor issues, the proximal segments of this specific pathway are relatively preserved.
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### Clinical Correlation
The patient presents a complex "mixed" picture:
* *The UMN Component:* Spasticity, increased tone, and spastic dysarthria (pseudobulbar palsy features) suggest significant involvement of the corticospinal and corticobulbar tracts, likely from the original febrile/seizure event (e.g., meningoencephalitis or acute disseminated encephalomyelitis - ADEM).
* *The LMN/Peripheral Component:* The NCS confirms a polyneuropathy. The *absent reflexes* (Left UL and bilateral knees) are likely explained by this peripheral nerve damage overriding the expected hyperreflexia of spasticity.
### Considerations for the "Citizen Scientist" Framework
Given the history of a febrile illness and the asymmetric, diffuse nature of the findings, one might investigate:
1. *Critical Illness Polyneuropathy (CIP):* If the initial illness involved a prolonged ICU stay or sepsis.
2. *Post-Viral/Inflammatory Brachial Plexopathy or Polyneuritis:* Given the asymmetry, particularly in the left upper limb.
3. *Nutritional/Metabolic Factors:* If the patient has had chronic mobility and feeding issues since the event.
The slow, effortful speech and inability to articulate complex Sanskrit-derived clusters (yuktaksharas) like "Yudhishthir" are classic for spastic dysarthria, reinforcing that the primary disability remains a high-level neurological insult, now complicated by a secondary peripheral neuropathy.
[3.36 pm, 08/05/2026] PPM 2: Unfortunately the PA was not added automatically. It's been a struggle with the current setup. Can they be manually added please?
[3.38 pm, 08/05/2026] PPM 1: @PA2 is currently the second PA as the entire family may not be able to handle the PaJR interface
@PPM3 @PA2 please confirm if the above assumption is true
The first patient advocate I was told was getting trained for the job of a fire fighter when this current tragedy struck one year back.



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