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Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
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Encephalitis l: Introduction01:19

Encephalitis l: Introduction

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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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Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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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...
18
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

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Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
19
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

14
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
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Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

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Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
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Related Experiment Video

Updated: Apr 28, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Endocrine encephalopathy.

King W Yong1, Steven Soule, Penny Hunt

  • 1RMO Unit, Christchurch Hospital, Private Bag 4710, Christchurch, New Zealand. kingwei.yong@gmail.com.

The New Zealand Medical Journal
|June 16, 2014
PubMed
Summary

Hashimoto's encephalopathy, a rare neurological disorder, can cause acute brain dysfunction. Prompt steroid treatment in a patient with positive thyroid antibodies led to a full recovery, highlighting its treatable nature.

Area of Science:

  • Neurology
  • Endocrinology
  • Immunology

Background:

  • Hashimoto's encephalopathy (HE) is an idiopathic autoimmune condition characterized by acute neurological dysfunction.
  • Diagnosis relies on excluding other causes of encephalopathy, detecting thyroid autoantibodies, and observing a response to corticosteroid therapy.

Observation:

  • A 59-year-old female presented with acute encephalopathy, including aphasia, weakness, and seizures, necessitating intensive care.
  • Extensive investigations ruled out other causes for her neurological decline.
  • High levels of thyroid autoantibodies and profound primary hypothyroidism were detected.

Findings:

  • The patient's seizures ceased promptly following high-dose intravenous methyprednisolone administration.
  • Thyroxine replacement therapy was initiated concurrently with steroid treatment.

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  • The patient experienced a complete neurological recovery after a gradual steroid taper.

    • Implications:

    • This case underscores the importance of considering Hashimoto's encephalopathy in patients with unexplained encephalopathy and positive thyroid antibodies.
    • Early diagnosis and aggressive immunosuppressive therapy, alongside thyroid hormone replacement, can lead to favorable outcomes.
    • Further research into the pathogenesis and optimal management of HE is warranted.