Difference between Vasogenic and Cytopathic Cerebral Edema

In this article, we will discuss the Difference between Vasogenic and Cytopathic Cerebral Edema. So, let’s get started.

  • Vasogenic Cerebral Edema
  • Produces focal signs and symptoms due to edema
  • Blood brain barrier remains open
  • Activated diffusion coefficient is increased
  • MRI shows increased interstitial fluid
  • Responds to steroids
  • It is associated with tumors, hemorrhage, abscess, meningitis, cerebral infarction
  • Cytopathic Cerebral Edema
  • The clinical signs are generalised, non-localising, i.e. convulsions, coma
  • Blood brain barrier is closed
  • Activated diffusion coefficient is reduced
  • MRI shows swollen cells
  • Does not respond to steroids
  • Seen in hemodialysis and ketoacidosis

Glasgow Coma Scale

In this article, we will discuss the Glasgow Coma Scale. So, let’s get started.

Glasgow Coma Scale

Systemic assessment of the unconsciousness patient is an important part of neurological examination. An application of Glasgow Coma Scale not only provides a grading of coma by numerical scale but allows serial comparisons to be made for prognostic information particularly in traumatic coma. This scale should be applied in each and every patient under observation and should be charted out from time to time for comparison.

Glasgow Coma Scale

Scale – Score

Eye opening (E)

  • Spontaneous – 4
  • To loud voice – 3
  • To pain – 2
  • Nil – 1

Best motor response (M)

  • Obeys – 6
  • Localises – 5
  • Withdrawal (flexion) – 4
  • Abnormal flexion – 3
  • Extensor response – 2
  • Nil – 1

Verbal response (V)

  • Oriented – 5
  • Confused, disoriented – 4
  • Inappropriate words – 3
  • Incomprehensible sounds – 2
  • Nil – 1

Coma Score (E+M+V)

  • Minimum – 3
  • Maximum – 15

Note: Patients with head trauma scoring 3 or 4 have an 85% chance of death or vegetative state; while scores above 11 indicate only 5-10% chance of death or vegetative state and 85% chance of moderate disability or good recovery. Intermediate scores have intermediate prognosis.

Pathogenesis of Brain Aneurysms

In this article, we will discuss the Pathogenesis of Brain Aneurysms. So, let’s get started.


The most common mechanism of aneurysms formation is thus a combination of several causes, starting with a congenital defect in the media at the bifurcation of cerebral vessels. These weak spots are present at branching of these vessels. Hemodynamic stress in the form of local turbulence of blood at this site causes hyperplasia and splitting of internal elastic lamina. This combination of a congenital defect with acquired loss of elastic membrane under the effect of blood pressure may predispose to outpouching of the fragmented elastica leading to saccular aneurysm formation which produces clinical features due to its rupture at the weakest spot. Aneurysms >7mm in diameter and those located at the top of basilar artery and at the origin of posterior communicating artery are at greater risk of rupture.

Sites of aneurysms

  • Anterior communicating artery (30.1%)
  • Middle cerebral artery (20%)
  • Internal carotid artery (7.5%)
  • Posterior communicating artery (25.1%)
  • Posterior inferior cerebellar artery (4.12%)
  • Basilator tip (7%)
  • Others (6.1%)

Provoking Factors for Migraine (Cluster Headache)

In this article, we will discuss the Provoking Factors for Migraine (Cluster Headache). So, let’s get started.


  • Food items such as cheese, dairy products, fruits, chocolates, ice-cream etc
  • Food additives such as caffeine (coffee), nitrates
  • Alcohol such as beer, red wine
  • Hormonal changes such as menstruation, pregnancy, ovulation, oral contraceptives
  • Visual triggers like bright lights, glare
  • Auditory triggers like noise and music
  • Olfactory triggers like perfumes, odours
  • Miscellaneous triggers such as hunger, sleep, exertion, head and neck trauma, stress and anxiety, cough.

Note: The clinical interview of an acute headache patient should be quick and systematic including onset, location of pain, character, severity, duration of pain, precipitating and relieving factors. Past history of similar episodes, history of trauma, exertional aspect of headache, physical tests done earlier, any treatment taken earlier and relief obtained therefrom should be noted.

Classification of Guillain-Barré Syndrome

In this article, we will discuss the Classification of Guillain-Barré Syndrome. So, let’s get started.



1. Acute inflammatory demyelinating polyradiculopathy (AIDP)


  • Demyelinating
  • Adults affected more than children
  • Anti-GM antibodies present (>50%)
  • Recovery rapid


2. Acute motor axonal neuropathy (AMAN)


  • Axonal damageChildren and young adults affected
  • Prevalent in China and Mexico
  • Anti-GD1a antibodies present
  • Recovery rapid


3. Acute motor-sensory axonal neuropathy (AMSAN)


  • Axonal damage
  • Uncommon, adults affected
  • Closely related to AMAN
  • Recovery slow


4. Miller-Fisher Syndrome


  • Demyelinating, uncommon
  • Affects children and adults
  • Ophthalmoplegia, ataxia and areflexia occur
  • Anti GQ-1b antibodies present (>90%)
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