The fixed brain is so much worse – with some brains, no amount of rinsing can remove the stench of formalin that makes your eyes and throat sting.
WARNING: I AM ABOUT TO BE SLIGHTLY DISGUSTING BELOW, but if you’re in this thread, you’re probably fine with what I am about to describe.
Of all the brains I had to cut up when I was learning neuropathology, there are two that still strike me because they were so unique and informative. (Of note, pathologists use food analogies, so preserved brains were like firm tofu or mushrooms, and the cauda equina at the end of the spine legitimately DOES look like ramen noodles stretched out. So if they’re your teachers, you pick up that bad habit.)
The first one was the brain of someone who had been declared brain-dead for three or four days before the family could bring themselves to withdraw care. Most brains that have been pickled in formaldehyde for the required number of weeks are sort of greyish, firm, easy to handle. This brain was purplish, soft, rotting, falling apart. You could tell that it had started to “decompose” prior to the person’s physical death.
The neuropathologist commented that once you’re braindead, your brain might as well be on the shelf next to your body for all the good it’s doing you. And you could *see* this. I know I say the brain is dead, but you could see how very dead the brain was!
The second memorable brain came from a small plane crash. I was hanging out in the lab, waiting for the neuropathologist to show, and one of the pathology fellows saw me and excitedly called me in to the next room to see “something cool.” (Note: never trust a pathologist’s definition of “cool”.)
An acute traumatic injury to the head and skull carrying a sudden concussive or shearing force transmitted to brain tissue. In addition to traumatic force, open traumatic injuries also involve fractures or penetration of the skull.
Head injuries are widely variable in severity, mechanism, and presentation, depending on the nature of the injury sustained.
In the awake patient, one may elicit a history of sudden impact or acceleration/deceleration injury, followed by brief loss of consciousness. Other symptoms may include amnesia, confusion, headache, photophobia, or hemiparesis. • Individuals may exhibit lethargy or decreased responsiveness, with decreased pupillary light reflex.
Post-traumatic seizures may be present.
Patients with severe injuries may present with cardiovascular instability, including bradycardia, other dysrhythmia, and hypotension.
Epidural hematomas are associated with a severe head impact. The classical presentation consists of a brief loss of consciousness, followed by a lucid interval, followed by rapid progression to decreased level of consciousness and coma.
Subdural hematomas, traumatic subarachnoid hemorrhage, and intraparynchymal hemorrhage each can result from traumatic injuries, but typically do not have a lucid interval.
Traumatic brain injury is widely variable in type, severity, and associated injuries. Primary injury includes direct injury of brain parenchyma from contusion, shearing, or penetrating injury from bone or foreign body. Secondary injury is defined as tissue damage that is caused by ischemia, edema, and inflammation that leads to transient or more permanent brain dysfunction. Secondary injury is exacerbated by vascular injury, hypoventilation, and associated cardiovascular events with or without intracranial hypertension (ICH).
Rupture of pre-existing arteriovenous malformation or aneurysm
Chronic subdural hematoma
Assess the patient’s airway, breathing, and circulation. Intubate the trachea and initiate mechanical ventilation if indicated. Note: If intubation of the trachea is indicated in a patient with a cervical spine injury, a technique that maintains spinal alignment (e.g., in-line cervical spine stabilization or fiberoptic intubation) must be used.
Provide supplemental oxygen if needed to avoid hypoxemia.
Rapidly examine the patient to identify additional life-threatening injuries.
Resuscitate the patient with normal saline or, if indicated, blood products. (Note: If massive transfusion is indicated for other injuries, consider infusing packed red blood cells, platelets, and fresh-frozen plasma in a 1:1:1 ratio.)
The cerebral perfusion pressure should be at least 60 mm Hg. Use vasopressors as necessary to achieve this goal (e.g., phenylephrine 100 mcg IV bolus or 0.5–1 mcg/kg/min). If ICH is suspected, increase the systemic blood pressure as needed to maintain CPP.
Administer mannitol 0.5–1.0 g/kg if ICH is suspected in the absence of disruption of blood-brain barrier.
If required, adjust mechanical ventilation to maintain PaCO2 30–35 mm Hg.
Request a consultation from the neurosurgic team to plan definitive therapy, including the need for ICP monitoring, CSF drainage, or emergency craniotomy.
Stroke is an emergency condition that occurs when the blood flow to the brain stops, commonly called as brain attack. Blood supply to the brain can get affected due to blocking of arteries reaching the brain or due to bleeding in or around the brain.
Thrombotic stroke occurs when an artery supplying blood to the brain gets blocked due to a clot, which can potentially cause damage to the brain.
Stroke is classified into three types based on the cause, which are, a blocked artery (ischemic stroke), bleeding in or around the brain (hemorrhagic stroke) and transient ischemic attack (a temporary episode).
Thrombotic stroke occurs from blockage of an artery supplying the neck or the brain. It is a type of ischemic stroke, as the disrupted blood supply can cause lack of oxygen and death of brain cells.
Ischemic stroke is of two types :
Thrombotic Stroke – Blockage of arteries resulting from a clot within the arteries supplying the brain.
Embolic Stroke – Blockage of arteries resulting from a clot elsewhere in the blood vessels of the body, which travel to the blood vessels in brain.
Transient ischemic attack (TIA) can also be a brief form of thrombotic stroke, in which temporary symptoms appear and is called a mini stroke. It too occurs when the clot formation is present in the arteries of the brain. The symptoms of TIA may be similar to stroke; may last for few minutes to hours but usually does not leave any permanent damage to the brain. It is considered as a warning sign of possible future stroke.
Types of Thrombotic Stroke
Thrombotic Stroke, which occurs due to blocking of arteries in the brain are also termed as cerebral thrombosis and it accounts for almost half of the cases of thrombotic stroke.
Thrombotic stroke or cerebral thrombosis are divided into types, which are related to the place of the clot in the artery. These are:
Large Vessel Thrombosis – Blockage occurs in the large arteries supplying the brain, like carotid artery or middle cerebral artery.
Small Vessel Thrombosis or Lacunar Stroke – Blockage occurs in one or more smaller and deeply penetrating arteries of the brain. It is also called lacunar infarct, (lacunar means a cavity or hole) and is commonly seen in people with diabetes or high blood pressure.
Causes of Thrombotic Stroke
The brain is supplied by large and small arteries carrying pure blood. The brain receives nutrients and oxygen through the blood reaching through these arteries. These blood vessels can get blocked due to various reasons, however, the commonest cause of artery blockage is narrowing or arteries due to atherosclerosis.
Atherosclerosis is a condition, in which, cholesterol and other substances, in the form of plaque, get deposited on the inner walls of arteries. This narrows the passage through which blood can flow. When arteries become very narrow, clots can develop due to collection of blood cells in an area. These clots (thrombus) when formed, block the artery, thus cutting off the blood supply to the brain. The brain cells feel deficient in nutrition and oxygen resulting in stroke. Hence the term thrombotic stroke.
Other causes that can lead to formation of blood clots in the arteries of brain include, certain traumatic injuries causing clot formation in the brain, blood clotting disorders or due to use of certain drugs and substance abuse. Occasionally, certain types of headaches, or migraines can cause excessive spasm of an artery of the brain, resulting in clot formation.
Certain risk factors that may increase the chances of having a thrombotic stroke include, high cholesterol, high blood pressure, diabetes, obesity, smoking and a family history or a previous history of stroke.
Symptoms of Thrombotic Stroke
Thrombotic stroke usually presents itself in different ways, depending on the areas of the brain affected and the severity of disturbance in blood flow to the brain. Depending on the area affected, particular functions controlled by the brain can get damaged in varying degrees.
Symptoms of thrombotic stroke can include sudden appearance of:
Headache, confusion or dizziness,
Vision disturbances or sudden loss of vision,
Weakness on one side of the body,
Difficulty or inability to speak or slurred speech,
Unstable walking, balancing problems and Co-ordination difficulty in hands and legs.
Treatment for Thrombotic Stroke
If the early signs of thrombotic stroke are sensed, immediate evaluation and treatment can be started, in which case, the chances of recovery are better. A thorough clinical examination, neurological assessment and related tests are done. Investigations like CT scan, Doppler ultrasound of the suspected arteries of brain and other tests as required are often performed.
Emergency treatment followed up with regular medications are required. Treatment includes medications to dissolve the clot and improve blood flow to the brain, which shows better results if given within 3 hours of beginning of symptoms. It is also necessary to treat underlying cause like high blood pressure or uncontrolled blood sugar in diabetes. In some cases, endovascular procedures in which the lodged thrombus or clot is removed through a surgical procedure, may be performed if appropriate.
Recovery Period for Thrombotic Stroke
Small thrombus that cause lack of blood supply for a short period and receiving timely treatment show better recovery. If blood supply is cut off for longer period, it can cause more damage. Depending on the symptoms and the damaged caused, rehabilitation may also be required.
Prognosis and recovery period depends on the size and location of the thrombus and severity and damage to the brain and other body parts.
Stroke, which occurs due to stopping of blood supply to the brain is often due to clot formation or bleeding in or around the brain. Clot formation in the arteries of brain occurs in ischemic stroke, while bleeding in or around the brain occurs in hemorrhagic stroke. Hemorrhagic strokes are comparatively less commonly seen and usually account for around 15% cases of stroke, but can cause death in about 40% of deaths due to stroke.
Hemorrhagic strokes are a result of rupture of a weak blood vessel, causing bleeding in the brain. Sometimes, bleeding can occur in the surrounding tissue, which can exert pressure on the brain. This can lead to decreased blood supply to some areas in the brain and damage to brain tissue, leading to a hemorrhagic stroke.
Types of Hemorrhagic Stroke
Hemorrhagic stroke is mainly classified into two types:
Intracerebral Hemorrhage – This is the commonest type of hemorrhagic stroke. In intracerebral hemorrhage, a blood vessel ruptures or bursts and bleeds into the brain tissue. The brain cells and tissue die resulting in damage to the part of the brain where bleeding occurs.
Subarachnoid Hemorrhage – This occurs when bleeding from a blood vessel occurs in to the space in between the brain and the surrounding tissue. This space is called subarachnoid space, hence the name subarachnoid hemorrhage.
Causes of Hemorrhagic Stroke
Hemorrhagic stroke is caused due to bleeding in the brain tissue or in the tissues around the brain. The common causes of bleeding in and around the brain includes
Aneurysm – This occurs when a weakened part of a blood vessel get enlarged, called as ballooning. If it is not attended to at the right time, the weakened part continues to weaken, causing thinning of the vessel wall until it ruptures and bleeds into the brain tissue. This causes intracerebral hemorrhage leading to hemorrhagic stroke. Aneurysm and resulting hemorrhagic stroke can occur due to high blood pressure.
Arteriovenous malformation (AVM) – It is a congenital condition, in which the blood vessels are abnormally formed or they are twisted in an abnormal manner. It usually affects the arteries and veins in the brain or spine. This affects the blood flow to the brain, also these blood vessels can rupture and cause bleeding into the brain. When blood vessels in the brain are malformed, it can result into intracerebral hemorrhage, while if the blood vessels in the surrounding tissue are involved, it results in subarachnoid hemorrhage, both resulting into hemorrhagic stroke.
Other Causes of Hemorrhagic Stroke Include:
Hypertension or high blood pressure,
Amyloidosis, in which a protein gets built up in the arteries of brain and cause easy bleeding.
Medicines like blood thinners, taken for treatment as anticoagulant therapy, thrombolytic therapy or for treating ischemic stroke.
Some risk factors that increase the risk of hemorrhagic stroke include:
High blood pressure
Previous history of stroke
Smoking and alcohol consumption
Substance or Drug abuse
Symptoms of Hemorrhagic Stroke
Hemorrhagic stroke may vary in its presentation and symptoms from person to person and also depends on the type of hemorrhage.
Intracerebral hemorrhage can present with severe headache, weakness or numbness in arms, face or legs, especially on one side, sudden nausea, vomiting, confusion and sometimes loss of consciousness. Seizures may also occur if the stroke has resulted from congenital malformation (AVM).
Subarachnoid hemorrhage may show symptoms of headache. Sudden, severe headache, nausea, vomiting, stiffness in the neck, sensitivity to light and loss of consciousness may be seen.
In either of types of hemorrhagic stroke, changes in level of alertness, difficulty in speech, swallowing problems, coordinated movements of hands and legs, difficulty in writing and reading, balance problems, changes in vision, blurring or loss of vision may also be noted.
Treatment of Hemorrhagic Stroke
Diagnosis is based on clinical examination and neurological assessment. Investigations like CT scan and MRI of brain help to reveal bleeding in and around the brain. Other tests like blood counts and clotting studies may be done. Cerebro-spinal fluid (CSF) may be examined, if required. Advanced tests to diagnose congenital malformations may be done.
Treatment for hemorrhagic stroke needs emergency medicines in order to prevent worsening of the situation or else it can be fatal. The aim of treatment for hemorrhagic stroke is to control bleeding and reduce the pressure caused by bleeding in the surrounding tissue.
Medications used to control bleeding are administered in people who have suffered from hemorrhagic stroke. In case, hemorrhagic stroke has resulted from consumption of blood thinners, medicines are given to counteract the effect. Additionally, anti-convulsants, anti-hypertensive drugs and diuretics to reduce intracranial pressure are used.
Subarachnoid hemorrhage (SAH) is a cerebrovascular accident in which bleeding occurs into the subarachnoid space. Extravasation of blood into the CSF can be caused by trauma or from nontraumatic bleeding of vascular defects, such as arteriovenous alformation (AVM) or from an arterial aneurysm.
Sudden onset, severe, “thunderclap” headache is a classic sign of SAH. “Worst headache of my life.”
Nausea and vomiting are common.
Confusion or agitation, decreased level of responsiveness, or transient loss of consciousness may occur.
Nuchal rigidity may be present.
Photophobia and seizure may occur.
Hypertension and elevated temperature are common signs.
Focal deficits from ischemia, such as cranial nerve palsy, may occur.
Kernig’s sign: resistance to full extension of leg at knee when hip is flexed.
Brudzinski’s sign: flexion of both hips and knees when neck is passively flexed.
Seventy to eighty-five percent of SAH events are secondary to aneurysmal bleeding, with the remainder of events caused by AVM, tumor, infection, or trauma. Arterial bleeding can rapidly increase ICP, potentially causing devastating neurologic impairment.
Headache of other etiology
Infection or abscess
Computed tomography scan without contrast, CT angiography: The Fisher grading scale, which describes the amount of blood observed on CT, helps to predict the occurrence of cerebral vasospasm.
Note: Diagnostic studies should not delay urgent surgical intervention.
Assess the patient’s airway, breathing, and circulation. Intubate the trachea and initiate mechanical ventilation if indicated.
Obtain large-bore peripheral IV access and insert an intra-arterial catheter for blood gas analysis and continuous blood pressure monitoring
Stabilize the blood pressure to achieve a CPP 60–70 mm Hg using vasopressors (e.g., phenylephrine 0.5 mcg/ kg/minute infusion or 100-mcg boluses) or intravenous short-acting beta blockers (e.g., labetalol) and/or calcium channel blockers (e.g., nicardipine; starting dose 5 mg/hour).
Consider moderate hypocapnia (PaCO2 25–30 mm Hg) to reduce ICP until definitive treatment is achieved.
Note: Hypercapnia decreases cerebral blood flow and worsens cerebral ischemia. This should only be used as a bridge to definitive treatment (e.g., surgical decompression).
Mild hypothermia is not indicated and does not improve neurologic outcome.
Request a consultation from the neurosurgical team to plan definitive therapy, which may include intravascular therapy (i.e., coiling or embolization) or surgical management (i.e., aneurysm clipping or AVM resection).
Close monitoring of neurologic status is imperative because re-bleeding may occur and carries a poor prognosis.
If vasospasm occurs, consider treatment with prophylaxis with nimodipine (60 mg by mouth or via nasogastric tube every 4 hours for 2 days), hypertensive hypervolemic hemodilution (“triple-H” therapy). Intravascular angioplasty, or stenting also should be considered.
A ventricular drain may be required for patients who develop obstructive hydrocephalus after SAH.
Additional management is guided by systemic complications, which catecholamine-induced cardiac abnormalities (e.g., dysrhythmia, myocardial infarction, heart failure), pulmonary hypertension and edema, and electrolyte disturbances (e.g., hyponatremia caused by syndrome of inappropriate anti-diuretic hormone [SIADH]).
Lumbar disk syndrome includes diseases resulting from disk disorder, either herniation or degenerative change (spondylosis). Massive disk protrusion may rarely lead to paralysis in the lower extremity, a condition termed cauda equina syndrome. Gradual narrowing of the spinal canal (lumbar stenosis), usually from spondylosis, may also cause lower extremity symptoms.
PHYSICAL FINDINGS & CLINICAL
Overlapping clinical syndromes that may result:
Mild herniation without nerve root compression
Herniation with nerve root compression
Cauda equina syndrome
Chronic degenerative disease with or without leg symptoms
Low back pain, often worsened by activity or coughing and sneezing
Local lumbar or lumbosacral tenderness
Paresthesias, usually unilateral
Restricted low back motion
Increased pain on bending toward affected side
Weakness and reflex changes (L4—knee jerk and quadriceps, L5—extensor hallucis longus, S1—ankle jerk and toe walking)
Sensory examination usually not helpful
Lumbar stenosis that possibly produces symptoms (pseudoclaudication), which are often misinterpreted as being vascular. Pseudoclaudication usually recovers quickly with sitting or spine flexion. Vascular disease is unaffected by spine position and is typically associated with atrophic skin changes and diminished pulses.)
Positive straight leg raising test if nerve root compression is present
Soft tissue strain or sprain
Degenerative arthritis of hip
Insufficiency fracture of hip or pelvis
In most cases the diagnosis can be established on a clinical basis alone.
Imaging is not warranted for most patients with acute low back pain.
Plain roentgenograms may be indicated within the first few weeks for persistent pain; they are usually normal in soft disk herniation, but with chronic degenerative disk disease loss of height of the disk space and osteophyte formation can occur.
MRI may be indicated in patients whose symptoms do not resolve or when other spinal pathology may be suspected.
Electrodiagnostic studies may confirm the diagnosis or rule out peripheral nerve disorders.
Short course (3 to 5 days) of limited physical activity for acute disk herniation with leg pain
Physical therapy for modalities plus a careful gradual exercise program. Physical therapists generally use the McKenzie method for the treatment of low back pain.
Lumbosacral corset brace during rehabilitation process in conjunction with exercise program is beneficial only in some cases.
Percutaneous electrical nerve stimulation may be beneficial in selected patients with chronic back pain.
ACUTE GENERAL Rx
Muscle relaxants for sedative effect
Epidural steroid injection for leg symptoms in selected patients