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If you are interested in neuroanesthesia....click on the link below.... It is the best site to learn about neuroanatomy and neurology ...                                                              Click here 

Intravenous administration of recombinant tissue plasminogen activator (rtPA) is currently the only  Food and Drug Administration approved treatment for ischemic stroke. The therapeutic window for IV rtPA in ischemic stroke is 3 h. As per the National Hospital Discharge Survey between 1999 and 2001 out of 1.79 million cases of stroke only 0.6% received rtPA. Intra-arterial (IA) thrombolysis is recommended when a patient misses the window for IV rtPA or has a contraindication for rtPA. Intraarterial thrombolysis is more effective in recanalization because of the delivery of the thrombolytic agent close to the site of occlusion (up to 70% recanalization rate). The therapeutic window for IA therapy extends up to 6h after a stroke. Combined IV rtPA and IA therapy also has been proposed. Mechanical removal of the clot (clot extraction) is another adjunct treatment for reperfusion/ recanalization in st...

There is no clear evidence of superiority of either mannitol or hypertonic saline at reducing intracranial pressure. One small trial suggested  mannitol was better , others have  favored hypertonic saline . The absolute differences of effects between agents have been quite small in these studies. If a ventricular drain is placed, CSF can be removed and intracranial pressure can be measured directly; this invasive approach carries a slight infection risk and has not been shown to improve outcomes. If a direct-pressure monitoring device is not in place, the goal of hyperosmolar therapy is to either: Increase the serum osmolarity initially to a target of  300-320 mOsm/L . Calculate osmolarity by (2 x Na) + (glucose / 18) + (BUN / 3), or use an  osmolarity calculator ,  or your lab’s true measured osmolality. Increase serum sodium to  145-150 mmol/L . Both these methods work whether using mannitol (an osmotic diuretic that causes generalized dehy...

Raised intracranial pressure (ICP) appears to be quite lethal: in traumatic brain injury patients, those with ICP > 40 mm Hg had a mortality of 56%, compared to 18% for those with ICP < 20 mm Hg. Most traumatic brain injuries causing long-term disability also initially presented with raised intracranial pressure. As volume increases inside the skull, intracranial pressure exponentially rises after it passes an inflection point of ~20-25 mm Hg. As ICP passes 50-60 mm Hg and approaches arterial pressure, global brain ischemia and eventual brain death result. The brain is 80% water, so using hyperosmolar agents to create an osmolar gradient between the inside of the brain and the systemic circulation has strong theoretical appeal. Hypertonic saline and mannitol are effective because they do not cross the blood-brain barrier (much), and thereby draw cerebrospinal fluid out of the cranium and fluid out of the injured brain, reducing pressure and further injury. In brain i...

Cerebral Blood volume (CBV)–PaCO2 curve is   flatter than  CBF-PaCO2.. (0.014 mL/100g/mm Hg)  See the foto Hence decreasing PaCO2 from 40 to 20 mm Hg will will decrease CBV to 2.8 mL/100g (a 28% change). This translates into a 10–14 mL fall in whole-brain volume. This look  as small number .... but in the light of Pressure Volume index  it will not be considered as small?? Shapiro et al. showed that the amount of fluid that must be rapidly injected into or withdrawn from the  intracranial space to change ICP tenfold (e.g., from 10 to 100 mm Hg) is normally ≈26 mL. This is called the pressure-volume index (PVI). However, PVI values in patients with mass lesions or closed head injuries may be as low as 5 mL. In such situations, a change in CBV of 10–15 mL would be enormous, and it is not surprising that hyperventilation has come to occupy such ...

Some high-yield, interesting points in the management of ICH. Myocardial “stunning” with depressed ejection fraction and pulmonary edema should be expected, due to a form of tako-tsubo cardiomyopathy, most commonly in subarachnoid hemorrhage. It’s not due to ischemia and gets better over weeks. Fever reduction  is recommended, although therapeutic cooling and targeted temperature management (induced hypothermia) have not been shown prospectively to improve outcomes. The increased metabolic demand of shivering caused by cooling concerns some experts. Vasospasm  after subarachnoid hemorrhage is common, predictable and can cause cerebral infarction if untreated. Thick blood in the subarachnoid space and bleeding in the lateral ventricles bilaterally signals higher risk for vasospasm.  Nimodipine  selectively vasodilates cerebral arteries and improves outcomes and should be given to all victims of SAH due to a ruptured aneurysm. A phase III study of pravastatin...

Sympathetic storming after traumatic brain injury remains one of the most dramatic clinical scene particularly in neurological units.   It occurs due to uncontrolled sympathetic surge with a diminish or unmatch parasympathetic response. According to Baguley criteria 5 out of the 7 clinical features should be present - tachycardia, tachypnea, hyperthermia, hypertension, dystonia, posturing, and diaphoresis. Various agents have been used for treatment like clonidine and Benzos   (article below) but haloperidol may worsen the symptoms. Dr. Blackman and coll. coined the term "PAID" - paroxysmal autonomic instability with dystonia- in Archives of Neurology March 2004. Please Click below to Read more about PAID.. Click Here

According to a study in J Trauma dec 2011 , the prescence of a skull fracture increases mortality in severe TBI by about 30%. The study Retrospective study of a total of 197 patients who had isolated severe TBI (GCS<9 at ED triage). The site was an university hospital. Paeds, multitrauma, traumatic cardiac arrest and no available CT images were exclusion criteria. Out of the 197 patients 46,7% had a skull fracture in the ED. 92 patients had a fractured skull while 105 patients comprised the non fractured group. These groups were compared for hospital mortality. Results Mortality in the skull fracture group was 64,1%. Mortality in the non skull fracture group was 31,4% Conclusion Skull bone fracture might double mortality in severe TBI. Not surprising. Skull fractures imply the head was hit with energy high enough to break skull bones. Consequently, one would expect more severe tissue injury. J Trauma. 2011 Dec;71(6):1611-4; discussion 1614

Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association click here

Normally ICP can rise to 80-100mmHg just when coughing/straining,think of neuro patients when they cough on the tube.... CSF is produced at 500 ml/day with a total of 150 ml in the system . This means there’s continuous circulation reabsorption. The two types of hydrocephalus are: obstructive – expect big lateral ventricles and normal 4th as there’s a blockage somewhere communicating – general big ventricles but all the piping is OK, it’s the filter/drain that’s blocked – think blood pluggin the arachnoid villi. one of the earliest clinical signs of raised ICP is reduced venous pulsation on fundoscopy – good luck with that… the old hyperventilation to reduce pCO2 and reduce ICP is a bit dodgy as it also does exactly what you don’t want it to do – it reduces cerebral blood flow. mannitol has two actions volume expander osmotic diuretic if osmolality is already >320 then mannitol won’t work. steroids work for vasogenic oedema from tumours but not anything ...

After  carotid endarterectomy,when patient unable to move one side.."it is STROKE until proven otherwise" For carotid endarterectomy, most centers report a perioperative stroke rate of between 3 and 5 per cent. The incidence of perioperative stroke is highest for patients with stroke, lower for patients with transient ischemic attack, and lowest in asymptomatic patients. Neurologic deficits occur most commonly in patients with poorly controlled preoperative hypertension or in those with hypertension or hypotension postoperatively.  Extremes of blood pressure that are outside the range of autoregulation of cerebral perfusion can contribute to cerebral ischemia. But most strokes will be surgical complications. (1) Per Sabiston, (Textbook of Surgery, 2001, p 1348), “neurologic deficits within the first 12 hours of operation are almost always the result of thromboembolic phenomena stemming from the endarterectomy site or damaged internal, common, or e...

Significant cardiac effects stemming from brain injury are well known, including alteration of cardiac rhythms, cardiac variability, and blood pressure regulation. Neurologic diseases such as parkinsonism, multiple sclerosis (MS), stroke, epilepsy, and tumors can have cardiac effects, although structural abnormalities on conventional MRI may be lacking. . MS is classically a disease of white matter, although it can also affect gray matter. Autonomic dysfunction is common, affecting as many as 50% of MS patients with symptoms that include orthostatic dizziness, bladder disturbances, temperature instability, gastrointestinal disturbances, and sweating. The effect of autonomic dysfunction on disease activity is unclear. Multiple brainstem lesions are evident on MRI, and may be linked to cardiac autonomic dysfunction. The variability of MS contributes to the difficul...

General anesthesia has an inhibitory effect on neurotransmission and, therefore, on the EP. The effect of anesthetics is greater on synaptic transmission than on axonal conduction. For this reason, responses recorded from polysynaptic pathways (e.g., cortical recordings) are affected by anesthesia to a much greater extent than those recorded from oligosynaptic pathways (e.g., spinal cord and subcortical recordings). ” All volatile anesthetics produce a dose-dependent increase in SSEP latency and a decrease amplitude. All volatile anesthetics, even at concentrations above 1.0 MAC, only minimally affect the sub-cortical waveform, resulting in high recordability and reliability. The effect of volatile anesthetics on cortical SSEP amplitude is compounded by nitrous oxide. Intravenous anesthetics generally affect SSEPs less than inhaled anesthetics do. Etomidate and ketamine increase SSEP amplitude. Propofol, midazolam, and barbiturates have a moderate depressant effect on SSEP am...

The incidence of VAE in posterior fossa surgery in the sitting position is reported to be 41– 45% with routine monitoring. However, with the use of Doppler ultrasound the reported incidence is as high as 42–85%. VAE often is clinically undetected and frequently not of serious concern in a healthy patient if the volume and rate of air entrainment are minimal. The amount of entrained air that is reported to be lethal in humans is approximately 300 mL. Significant morbidity and mortality from VAE is now <1%  predominantly as a result of better monitoring techniques, early detection, and prompt intervention. Sitting position is contraindicated in patients with documented intracardiac defects or arteriovenous malformations because of the risk of paradoxical air embolism . Patent foramen ovale is the most common congenital defect associated with a paradoxical air embolus. Children generally have greater clinically significant hemodynamic derangement from VAE than do adults...

Delayed cerebral ischemia ( DCI ) is the most common cause of secondary neurologic injury in patients with aneurysmal subarachnoid hemorrhage ( SAH ). Intravascular volume depletion is one of several factors thought to cause, or worsen, DCI . Pulmonary edema frequently occurs in patients with SAH . A recent study in patients with SAH and pulmonary edema demonstrated that many were not volume overloaded.  In fact, many were intravascularly volume depleted. Think twice about aggressive diuresis in patients with SAH and pulmonary edema, as this may exacerbate volume depletion and may worsen DCI . References Scalfani MT, Diringer MN. Year in review 2010: Critical Care - neurocritical care. Crit Care 2011;15:237

The Use of steroids in Spinal cord trauma/injury is controversial topic ,some still belief it is helpful, and surely there are opponents who belief the opposite..the question what is the evidence? here were we are putting some of the literature findings...some findings support and another don't.. The original NASCIS trial (NASCIS I) found no difference in motor function or pinprick/sensation from baseline with IV methylprednisolone use, but the doses used were much lower than the doses used in the animal studies that first suggested a possible benefit.  Therefore, NASCIS II was performed to look at high dose methylprednisolone in acute spinal cord injury.  Patients received either methylprednisolone, naloxone, or placebo within the first twelve hours of injury.  The methylprednisolone was high dose and given for 24 hours.  Overall there was no benefit in the methylprednisolone group, but sub-group analysis showed a small benefit in motor function in the patien...

Owing partly to the assumption that adverse neurologic events were specifically related to the use of extracorporeal cardiopulmonary bypass, techniques were developed for performing CABG without the use of cardiopulmonary bypass (i.e., off-pump surgery). However, recent large, prospective, randomized studies comparing the rate of adverse neurologic outcomes after conventional on-pump surgery with the rate after off-pump surgery have not shown a significant risk reduction associated with the use of off-pump surgery. Consequently, efforts to reduce the incidence of postoperative neurologic injury have begun to focus on patient-related risk factors, such as the degree of atherosclerosis of the aorta, the carotid arteries, and the brain, rather than procedure-related variables

Begin with induction dose of propofol, 1 mg/kg (patient typically apneic for few seconds only; able to breathe spontaneously reasonably quickly); then, infuse with propofol, 100 µg/kg and titrate up or down as necessary; monitor capnography so patient breathing spontaneously but generally unresponsive to voice. sleep 1 —surgeon performs local anesthetic infiltration, applies pins, and places urinary catheter. patient awakened and allowed to remain awake during placement of drapes (knows what to expect during next awake period; gets used to manipulation); repeat propofol induction and infusion procedure (pin head holder then locked down).   sleep 2 —surgeon performs craniotomy and dural reflection. stop propofol infusion and allow patient to awaken (perform surface mapping or EEG recording). sleep 3 — onc e areas to be resected are identified, anesthetize patient once resection complete, patient reawakened (if EEG monitoring necessary, electrodes reapplied to verify elim...

All patients with severe head injury and moderate head injury whose progress can not be followed by serial neurological evaluation should be considered for ICP monitoring. The Brain Trauma Foundation guidelines suggest ICP-monitoring should be considered in the following settings: · Severe head injury (GCS 3-8) + abnormal CT scan · Severe head injury (GCS 3-8) + normal CT scan if 2 of the following are present : o Age > 40 o BP < 90 mmHg o Abnormal motor posturing Individual intracranial pressure monitors have different limitations: · Intraparenchymal monitors/subdural bolts: can not be calibrated, subject to “drift”, do not allow CSF drainage for control of ICP · Require expertise and resource availability for placement · Infection No RCTs have demonstrated that ICP-guided therapy improves patient centred outcomes. Some observational studies have noted an association between ICP guided management and prolonged length of stay (Cramer, 2005) and worse outcome (Shafi, 2008).

Cardiovascular: - I nitial parasympathetic discharge : prominent during the first ECT treatment, bradycardia , asystole , premature atrial/ventricular contractions. Hypotentsion - Sympathetic discharge follows : tachycardia, hypertension, PVCs, rarely VT. Usually tachycardia is self limited, peaking at 2 minutes -EKG changes: ST-segment depression and T-wave inversion Central Nervous System: -headache, short-term memory loss, confusion, agitation, increased blood flow and CMR, elevated intraocular pressure Neuroendocrine: -increased stress hormones: ACTH, cortisol, vasopressin, prolactin, GH, epinephrine and NE -improvement in NIDDM and hyperglycemia with IDDM Gastrointestinal tract: -elevated intragastric pressure