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Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...
Tetanus01:29

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Tetanus is a life-threatening neurological disorder characterized by persistent muscle contractions and spastic paralysis. It is caused by Clostridium tetani, a motile, Gram-positive, rod-shaped, obligate anaerobe. These bacteria produce terminal endospores, giving them a distinctive “lollipop” or “tennis-racket” appearance. They thrive in anaerobic environments, such as those found in deep puncture wounds.Once introduced into the body, the spores germinate into vegetative cells. These cells...
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Rigidity and myotonia are distinct abnormalities of muscle tone that affect resistance and relaxation during movement. Although both involve altered muscle contraction, they arise from different neurological and muscular mechanisms.CharacteristicsRigidity is characterized by uniform resistance to passive movement across the entire range, independent of speed, affecting flexors and extensors equally. It may appear as lead-pipe rigidity (smooth, constant resistance) or cogwheel rigidity...

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Related Experiment Video

Updated: Jun 3, 2026

Implantation of Osmotic Pumps and Induction of Stress to Establish a Symptomatic, Pharmacological Mouse Model for DYT/PARK-ATP1A3 Dystonia
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Oromandibular dystonia in encephalitis.

J Kalita1, U K Misra, P K Pradhan

  • 1Nuclear Medicine, Sanjay Gandhi Post Graduate Medical Sciences, Lucknow, India. jayanteek@yahoo.com

Journal of the Neurological Sciences
|March 16, 2011
PubMed
Summary

Oromandibular dystonia (OMD) in patients following encephalitis, primarily Japanese encephalitis, often involves specific brain regions. While many patients experience severe symptoms, some show improvement over time.

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Area of Science:

  • Neurology
  • Neuroscience
  • Infectious Diseases

Background:

  • Oromandibular dystonia (OMD) is a movement disorder affecting the jaw, tongue, and facial muscles.
  • Encephalitis, particularly Japanese encephalitis (JE), can lead to secondary OMD.
  • Understanding the clinical and neuroimaging features of OMD post-encephalitis is crucial for diagnosis and management.

Purpose of the Study:

  • To describe the clinical and MRI findings in patients with OMD secondary to encephalitis.
  • To investigate the neuroanatomical correlates of OMD in this patient cohort.
  • To assess the natural course and outcomes of OMD following encephalitis.

Main Methods:

  • Retrospective analysis of 17 patients with OMD due to Japanese encephalitis (14) or nonspecific encephalitis (3).
  • Clinical assessment of OMD severity and functional status (e.g., need for tube feeding).
  • Cranial MRI and SPECT imaging to evaluate brain structural abnormalities and perfusion.

Main Results:

  • The median age of patients was 14 years, with 9 females. Jaw-opening OMD occurred in 8 patients, and jaw-closing OMD in 9.
  • 11 patients were anarthric and required tube feeding, indicating significant severity.
  • MRI revealed abnormalities in the thalamus (9), substantia nigra (10), and other basal ganglia structures in most patients. SPECT showed hypoperfusion in thalamus and basal ganglia.
  • OMD showed improvement in 8 patients within 6 months, with complete regression in 6.

Conclusions:

  • OMD following encephalitis is predominantly associated with Japanese encephalitis.
  • Thalamus and substantia nigra are frequently affected brain regions in OMD secondary to encephalitis.
  • A significant proportion of patients with OMD post-encephalitis experience clinical improvement over time.