THE SUCCESS OF KETAMINE IN REFRACTORY SEIZURES, WHERE BENZODIAZEPINES FAIL

🔴In status epilepticus is there is a reduction in expression of “benzodiazepine-sensitive” GABAA-R d2 subunits 

🔴Also there is a 20-fold loss of potency in benzodiazepine receptors after 30 minutes.

🔴But there is an increase in the expression of excitatory NMDA receptors occurs, leading to seizure propogation

🔴Continued seizures result in BBB dysfunction facilitating leakage of albumin into the CNS, with a resultant proconvulsant effect by stimulating astrocytes to release NMDA and causing cerebral vasoconstriction.

🔴With continuing seizures, inhibitory GABA receptors are internalized in clathrin-coated vesicles, and excitatory NMDA receptors are mobilized to the membrane. This receptor trafficking may result in decreased inhibitory control and increased excitation that may foster status epilepticus. 

🔴The strong NMDA antagonist effect of ketamine has anticonvulsant effects and has the potential to prevent glutamate-mediated neurotoxicity. 

🔴Williams et al used a dose of 5 mg/kg/h in patients to control the seizures. The literature shows that doses as high as 7.5 mg/kg/h used for up to 14 days were safe.

🔴"With ketamine use, a concern about increasing intracranial pressure has been raised in ventilated patients. However, ketamine may not significantly elevate intracranial pressure and may provide some degree of neuroprotection by inhibiting the NMDA-receptor activation and interfere with the inflammatory response to injury when used in typical sedative or anesthetic doses."

🔴Ketamine may be the ideal agent for the control of seizure in patients with refractory seizures and septic shock in the intraoperative setting.

REFERENCE:

Use of Ketamine for Control of Refractory Seizures During the Intraoperative Period ; Williams, George W. MD; Cheng, Yuen C. MD; Sharma, Aanchal MD, Journal of Neurosurgical Anesthesiology, October 2014, Volume 26, Number 4

Predictors of mortality after subarachnoid hemorrhage

<Ⓜ️nemo : "POOR PreDICTOR"

P͞͞O͞͞O͞͞R͞͞  neurologic condition at hospital admission, a function of rate and volume of bleed

P͞͞R͞͞E͞͞existing illness

D͞͞epressed level of consciousness after initial bleed

I͞͞ncreased blood pressure

C͞͞irculation affected: if Basilar 

T͞͞hick clot in the brain substance or ventricles on initial computed tomographic scan

O͞͞lder age

R͞͞epeat hemorrhage

PAIN IN GUILLAIN BARRE SYNDROME

✔️GBS a number of different subtypes

✔️The most common is an acute inflammatory demyelinating polyradiculoneuropathy 

✔️More than half of patients report severe pain. 

✔️Severe widespread neuropathic pain may be described, often without the features of a peripheral neuropathy, as well as musculoskeletal pain. 

✔️May sometimes have severe acute pain, 

✔️Treatment with systemic ketamine and/or lidocaine as well as gabapentin/pregabalin and carbamazepine may be of benefit in the acute phase (ANZCA and FPM, 2010).

Ref: Acute Pain Management: A practical guide,4/e, Pamela E. Macintyre , Stephan A. Schug

Predisposing factors for rebleeding after Aneurysmal SAH

🔹Large volume of blood in the subarachnoid space from the initial SAH

🔹Poor neurologic status owing to the devastation caused by the initial SAH

🔹Short interval from the initial hemorrhage

🔹Female gender: women rebleed twice as frequently as men

🔹Older age and poor general medical condition

🔹Systemic hypertension: the risk of rebleeding is directly related to the patient's systolic blood pressure

🔹Multiple previous episodes of rebleeding that increase the likelihood of subsequent rupture and death

🔹Presence of either an intracerebral or intraventricular hematoma

🔹Abnormal clotting parameters

🔹Posterior circulation aneurysms

Ref: Philippa Newfield, Audrée A. Bendo, Handbook of Neuroanesthesia, 4th Edition, 2007 Lippincott Williams & Wilkins

💹EEG IN ACUTE INTOXICATIONS

💠Barbiturates 

Usually they produce fast activity (15-35/sec ) In the acute overdose, these type of fast activity may still be present, with some deceleration (10-16/sec). The inability of the cortex to produce, barbiturate induced fast activity has been described as a sign of cerebral impairment 

💠Benzodiazepines 

〰Fast activity (15-25/sec) range

💠Tricyclic Antidepressants

〰Widespread and poorly reactive 8-10/sec activity with paroxysmal discharges

💠Lithium Carbonate

〰Marked slowing, paroxysmal bursts, and triphasic waves

💠Neuroleptic drugs ( phenothiazines, butyrophenones)

〰Diffuse slow activity; often with burst like appearance or intermingled with paroxysmal discharges. Fast frequencies are absent

💠Opioids:

〰Relatively little repercussion in EEG; if produces profound coma → diffuse slowing

💠Carbon monoxide

〰Massive slowing (1-4/sec)

💠Ethyl alcohol

〰Effect on EEG is mild

💠Methyl alcohol

〰EEG slowing is correlated with acidosis rather than blood and CSF methanol levels

💠Organophosphorous compounds

〰Initially, fast EEG activity may be supplanted by slow activity 

Ref: EEG and intensive care medicine : RB Hansen, E Niedermeyer; Prog neurol Surg, vol 12, pp 105-145 ( Karger, Basel 1987)

📝BRAIN TUMOURS-SYMPTOMATOLOGY

📌Contralateral signs :  are associated with lesions in the posterior frontal area (motor) or anterior parietal lobe (sensory)

📌Lesions in the dominant hemisphere: Aphasia

📌Lesions in the non dominant hemisphere: Apraxia

📌Temporal lobe lesions : Focal seizures with auras and visual field defects

📌Frontal lobe lesions : Altered cognitive functioning and subtle personality changes

📌Subfrontal lesions : Anosmia

📌Sellar and Parasellar lesions: Visual field and Acuity problems , hypopituitarism, oversecretion syndromes (Cushing Syndrome, Acromegaly)

📌Tumours in relation to Ventricular system : Hydrocephalus , Raised ICP

📌Tumours of the brainstem and cerebellopontine angle : Cranial nerve palsies , long tract signs , secondary hydrocephalus

📌Lesions of Cerebellar vermis : Truncal ataxia

📌Lesions in Cerebellar hemisphere: Appendicular signs such as incoordination and nystagmus 

Reference:

Page :617-618, Bailey and Love’s , SHORT PRACTICE OF SURGERY , 24 th edition