Hypoxemic - Anoxic Brain injury

Several factors are important prognostic findings, particularly in patients who have not received significant sedation The outcome of hypoxic–ischaemic brain injury worsens if:

• The patient has been in coma (ie, unresponsive) for >6 h.
• There are no spontaneous limb movements or localisation to painful stimuli in the initial stages.
• There is prolonged loss of pupillary responses (provided atropine has not been administered).
• There is sustained conjugate eye deviation (upgaze or downgaze).
• There are specific forms of abnormal eye movements (eg, upbeat and downbeat nystagmus, ping pong gaze or period alternating nystagmus).
• There are myoclonic seizures.
• Lower cranial nerve function is involved (eg, absent cough and gag reflexes).

FOUR score (Full Outline of UnResponsiveness)

Eye response	4	Eyelids open, tracking or blinking to command
	3	Eyelids open but not tracking
	2	Eyelids closed but open to a loud voice
	1	Eyelids closed but open to pain
	0	Eyelids remain closed with pain
Motor response	4	Thumbs-up, fist or peace sign
	3	Localising to pain
	2	Flexion response to pain
	1	Extension response to pain
	0	No response to pain, or generalised myoclonic status
Brainstem reflexes	4	Normal pupil and corneal reflexes present
	3	One pupil wide and fixed
	2	Pupil or corneal reflexes absent
	1	Pupil and corneal reflexes absent
	0	Absent pupil, corneal and cough reflex
Respiration	4	Not intubated, regular breathing pattern
	3	Not intubated, Cheyne–Stokes breathing pattern
	2	Not intubated, irregular breathing pattern
	1	Breaths above ventilator rate
	0	Breaths at ventilator rate, or apnoea

http://pn.bmj.com/content/11/1/4.full#F2

basal cistern

vasogenic vs Cytotoxic Edema

brainstem syndrome

Claude's syndrome is caused by midbrain infarction as a result of occlusion of a branch of the posterior cerebral artery. This lesion is usually a unilateral infarction of the red nucleus and cerebral peduncle, affecting several structures in the midbrain including:

Structure damaged	Effect
dentatorubral fibers	contralateral ataxia
corticospinal tractfibers	contralateral hemiparesis
corticobulbar tractfibers	contralateral hemiplegia of lower facial muscles, tongue, and shoulder
oculomotor nerve fibers	ipsilateral oculomotor nerve palsy with a drooping eyelid and fixed wide pupil pointed down and out; probablediplopia

Bnedikt:
It is characterized by the presence of an CN III oculomotor nerve palsy and cerebellar ataxia including tremor. Neuroanatomical structures affected include CNIII nucleus, Red nucleus, corticospinal tracts, brachium conjunctivum, and cerebellum. It is very similar in etiology, morphology and clinical presentation to Weber's syndrome; the main difference between the two being that Weber's is more associated with hemiplegia (i.e. paralysis), and Benedikt's with hemiparesis (i.e. weakness).

Foville's syndrome is caused by the blockage of the perforating branches of the basilar artery in the region of the brainstem known as thepons.^[1]

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus.

Millard-Gubler syndrome

Symptoms result from the functional loss of several anatomical structures of the pons, including the sixth and seventh cranial nerves and fibers of the corticospinal tract. Paralysis of the abducens (CN VI) leads to diplopia, internal strabismus, and loss of power to rotate the affected eye outward), and disruption of the facial nerves (CN VII) leads to symptoms including flaccid paralysis of the muscles of facial expression and loss of the corneal reflex. Disruption of the corticospinal tract leads to contralateral hemiplegia of the extremities.

It is a form of "crossed hemiplegia," as the paralysis of muscles controlled by the facial nerve occurs on the same side as the lesion, while the hemiplagia of muscles below the neck occurs on the opposite side as the lesion.

wallenberg syndrome

http://www.medscape.org/viewarticle/730607?src=cmemp 

learning brain CT

http://www.neurosurvival.ca/ComputerAssistedLearning/readingCTs/tutorial.htm

http://www.neurosurvival.ca/ComputerAssistedLearning/readingCTs/how_to_read_a_ct_image.htm

What happens to brain when we are unconscious?

What happens to your brain as it slips into unconsciousness? A new technique allows researchers to view real-time 3-D images of a patient undergoing anesthesia using the drug propofol, and the findings show that consciousness isn't suddenly switched off, but rather fades as though a dimmer is being dialed down.

The research also suggests that consciousness resides in the connections between multiple parts of the brain, not in any single region. The images show that changes in the anesthetized brain start in the midbrain, where certain receptors for a neurotransmitter called GABA are plentiful.

Drugs like propofol act on these GABA A receptors, mimicking and enhancing the effects of GABA, which inhibits cellular activity. From the midbrain, changes move outward to affect the whole brain; as propofol's message spreads from region to region, consciousness dissolves.

"Our jaws ricocheted off the ground, and I won't say the words we used when we first saw the video," says lead author Dr. Brian Pollard, professor of anesthesia at the University of Manchester, who presented the results at the European Anesthesiology Conference in Amsterdam on Saturday. "We just sat there and stared, dumbfounded and kept repeating it. We're the first people in the world ever to see the brain becoming unconscious, that's quite a sobering thought."

Although anesthesia has been widely used since 1846, when a dentist first demonstrated the effects of ether at Massachusetts General Hospital, until recently very little has been understood about how it works. Even though scientists know that anesthetic drugs like propofol affect GABA in the brain, how that actually eliminates consciousness still remains a mystery.

Pollard explains, however, that propofol alters "the balance between inhibition and excitation in the brain," shifting the balance of activity toward the inhibitory circuits. At first, this produces a paradoxical result.

"When inhibition is inhibited, you first move into a stage of excitation or mania," he says, noting that this usually occurs too quickly to be observed with modern anesthesia. But the brief sense of euphoria that some people experience before losing consciousness from propofol may reflect this loss of inhibition (and may also account for Michael Jackson's taste for the drug).

"You then begin to inhibit the excitation and the patient becomes more sedated and loses consciousness," he says. That's why in the video the brain appears to become more active while unconscious: it's showing the increased action in inhibitory circuits.

Read more: http://healthland.time.com/2011/06/15/real-time-video-first-look-at-a-brain-becoming-unconscious-under-anesthesia/#ixzz1PxfDpaRN

SAH treatment

Medical stabilization is aimed at preventing early complications, including brain edema, hydrocephalus, and rebleeding, as well as the late complication of vasospasm. Treatment options include bed rest with elevation of the head of the bed to 30 degrees, nimodipine (a calcium channel blocker to prevent vasospasm), seizure prophylaxis, antiemetics, analgesia, and labetalol or other agents as needed for blood pressure control.