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Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
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Cranial nerves are responsible for transmitting motor and sensory information between the brain and various parts of the body. There are twelve pairs of cranial nerves, with the first six being essential in sensory perception, motor control, and autonomic functions related to the head and neck.
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Pain01:20

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Pain serves as a critical warning signal that alerts the body to potential or actual harm. When mechanical pressure on the skin is intense, such as from a sharp pinch, the sensation transitions from touch to pain. Similarly, extreme temperatures, like a hot pot handle, convert the sensation of heat into pain. Pain can also result from overstimulation of other senses, such as blinding light, loud noise, or the intense heat from habañero peppers. This ability to sense pain is essential for...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
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Minimally Invasive Surgical Decompression of Occipital Nerves
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Central pain in the face and head.

Jörgen Boivie1

  • 1Department of Neurology, University Hospital, Uppsala, Sweden. jrgen.boivie@telia.com

Handbook of Clinical Neurology
|September 7, 2010
PubMed
Summary

Central neuropathic pain arises from central nervous system lesions, often delayed after stroke or affecting legs in multiple sclerosis. Treatments like antidepressants and antiepileptics show limited efficacy.

Area of Science:

  • Neurology
  • Pain Medicine
  • Neuroscience

Background:

  • Central neuropathic pain (CNP) is a debilitating condition resulting from lesions in the central nervous system (CNS).
  • Conditions like stroke, multiple sclerosis (MS), and spinal cord injury are common causes of CNP.
  • The location and nature of CNS lesions significantly influence pain characteristics and prevalence.

Purpose of the Study:

  • To summarize the etiology, clinical presentation, and treatment of central neuropathic pain.
  • To highlight the variability in pain quality and location based on lesion type and site.
  • To discuss the challenges in treating central neuropathic pain due to poor analgesic response.

Main Methods:

  • Review of existing literature on central neuropathic pain.

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  • Analysis of clinical data regarding lesion location and pain manifestation in stroke and multiple sclerosis patients.
  • Summary of current treatment strategies and their effectiveness.

    • Main Results:

    • Central neuropathic pain can be induced by various CNS lesions, with location being a critical factor.
    • Stroke-induced pain is often delayed, constant, and hemipain (75%), while MS-related pain predominantly affects the legs (87%).
    • Central pain exhibits diverse qualities, is linked to sensory abnormalities, and responds poorly to conventional analgesics.

    Conclusions:

    • Lesions in spinothalamic pathways are hypothesized to cause central pain, but unknown factors contribute to its development.
    • First-line treatments include tricyclic antidepressants and antiepileptic drugs, despite generally poor responses.
    • Further research is needed to understand the underlying mechanisms and improve therapeutic outcomes for central neuropathic pain.