Severe hypertension, defined as blood pressure greater than 180/120 mmHg, is a condition that prevents the use of thrombolysis. In order to proceed with thrombolysis, it is necessary to lower the patient’s blood pressure to below this level within the designated time frame. Oral medications are unlikely to work quickly enough, so an intravenous antihypertensive agent is required.

One commonly used agent in these situations is labetalol, which is administered intravenously at a dose of 10 mg over 1-2 minutes. This dose can be repeated if necessary, or an infusion can be set up to deliver a continuous dose of 2-8 mg per minute. Once the blood pressure is reduced to less than 180/105 mmHg, thrombolysis can be safely performed.

Alternatively, a nitrate infusion, such as Isoket, can be used in patients who cannot tolerate beta-blockers due to contraindications like asthma, heart block, or cardiac failure. This provides an alternative option for lowering blood pressure in these individuals.

The meninges refer to the protective tissue layers that surround the brain and spinal cord. These layers, along with the cerebrospinal fluid (CSF), work together to safeguard the central nervous system structures from physical harm and provide support for the blood vessels in the brain and skull.

The meninges consist of three distinct layers: the outermost layer called the dura mater, the middle layer known as the arachnoid mater, and the innermost layer called the pia mater.

There are three types of hemorrhage that involve the meninges. The first is extradural (or epidural) hemorrhage, which occurs when blood accumulates between the dura mater and the skull. The second is subdural hemorrhage, where blood gathers between the dura mater and the arachnoid mater. Lastly, subarachnoid hemorrhage happens when blood collects in the subarachnoid space, which is the area between the arachnoid mater and the pia mater.

The symptoms and signs of strokes can vary depending on which blood vessel is affected. Here is a summary of the main symptoms based on the territory affected:

Anterior cerebral artery: This can cause weakness on the opposite side of the body, with the leg and shoulder being more affected than the arm, hand, and face. There may also be minimal loss of sensation on the opposite side of the body. Other symptoms can include difficulty speaking (dysarthria), language problems (aphasia), apraxia (difficulty with limb movements), urinary incontinence, and changes in behavior and personality.

Middle cerebral artery: This can lead to weakness on the opposite side of the body, with the face and arm being more affected than the leg. There may also be a loss of sensation on the opposite side of the body. Depending on the dominant hemisphere of the brain, there may be difficulties with expressive or receptive language (dysphasia). In the non-dominant hemisphere, there may be neglect of the opposite side of the body.

Posterior cerebral artery: This can cause a loss of vision on the opposite side of both eyes (homonymous hemianopia). There may also be defects in a specific quadrant of the visual field. In some cases, there may be a syndrome affecting the thalamus on the opposite side of the body.

It’s important to note that these are just general summaries and individual cases may vary. If you suspect a stroke, it’s crucial to seek immediate medical attention.

The most probable diagnosis in this case is a subarachnoid haemorrhage (SAH).

When assessing patients who present with an SAH, there may be focal neurological signs that can indicate the potential location of the aneurysm. Common sites for aneurysms include the bifurcation of the middle cerebral artery, the junction of the anterior communicating cerebral artery, and the junction of the posterior communicating artery with the internal carotid artery. If there is complete or partial palsy of the oculomotor nerve, it suggests the rupture of a posterior communicating artery aneurysm.

While hypertension is a risk factor for SAH, a significant increase in blood pressure may occur as a reflex response following the haemorrhage.

The first-line investigation for SAH is a CT head scan, which can detect over 95% of cases if performed within the first 24 hours. The sensitivity of the scan increases to nearly 100% if done within 6 hours of symptom onset. If the CT head scan is negative and there are no contraindications, a lumbar puncture (LP) should be performed to diagnose SAH. It is recommended to perform the LP at least 12 hours after the onset of headache. It is important to note that approximately 3% of patients with a negative CT scan will be confirmed to have had an SAH after undergoing an LP.

Tonsillar herniation occurs when the cerebellar tonsils are pushed through the foramen magnum. This condition is characterized by a decrease in consciousness, respiratory arrest, and flaccid paralysis.

Further Reading:

Intracranial pressure (ICP) refers to the pressure within the craniospinal compartment, which includes neural tissue, blood, and cerebrospinal fluid (CSF). Normal ICP for a supine adult is 5-15 mmHg. The body maintains ICP within a narrow range through shifts in CSF production and absorption. If ICP rises, it can lead to decreased cerebral perfusion pressure, resulting in cerebral hypoperfusion, ischemia, and potentially brain herniation.

The cranium, which houses the brain, is a closed rigid box in adults and cannot expand. It is made up of 8 bones and contains three main components: brain tissue, cerebral blood, and CSF. Brain tissue accounts for about 80% of the intracranial volume, while CSF and blood each account for about 10%. The Monro-Kellie doctrine states that the sum of intracranial volumes is constant, so an increase in one component must be offset by a decrease in the others.

There are various causes of raised ICP, including hematomas, neoplasms, brain abscesses, edema, CSF circulation disorders, venous sinus obstruction, and accelerated hypertension. Symptoms of raised ICP include headache, vomiting, pupillary changes, reduced cognition and consciousness, neurological signs, abnormal fundoscopy, cranial nerve palsy, hemiparesis, bradycardia, high blood pressure, irregular breathing, focal neurological deficits, seizures, stupor, coma, and death.

Measuring ICP typically requires invasive procedures, such as inserting a sensor through the skull. Management of raised ICP involves a multi-faceted approach, including antipyretics to maintain normothermia, seizure control, positioning the patient with a 30º head up tilt, maintaining normal blood pressure, providing analgesia, using drugs to lower ICP (such as mannitol or saline), and inducing hypocapnoeic vasoconstriction through hyperventilation. If these measures are ineffective, second-line therapies like barbiturate coma, optimised hyperventilation, controlled hypothermia, or decompressive craniectomy may be considered.

The median nerve originates from the lateral and medial cords of the brachial plexus and receives contributions from the ventral roots of C5-C7 (lateral cord) and C8 and T1 (medial cord). It serves both motor and sensory functions.

In terms of motor function, the median nerve innervates the flexor muscles in the anterior compartment of the forearm, excluding the flexor carpi ulnaris and a portion of the flexor digitorum profundus, which are instead innervated by the ulnar nerve. Additionally, it innervates the thenar muscles and the lateral two lumbricals.

Regarding sensory function, the median nerve gives rise to the palmar cutaneous branch, which provides innervation to the lateral part of the palm. It also gives rise to the digital cutaneous branch, which innervates the lateral three and a half fingers on the palmar surface of the hand.

Within the forearm, the median nerve branches into two major branches. The first is the anterior interosseous nerve (AIN), which supplies the flexor pollicis longus, pronator quadratus, and the lateral half of the flexor digitorum profundus. The second is the palmar cutaneous branch, which provides sensory innervation to the skin of the radial palm.

Differentiating between damage to the median nerve at the elbow and wrist can be done by considering these two branches. Injury at the elbow affects these branches, while injury at the wrist spares them. It is important to note that the palmar cutaneous branch travels superficially to the flexor retinaculum and therefore remains functional in carpal tunnel syndrome. However, it can be damaged by laceration at the wrist.

A comparison of median nerve lesions at the wrist and elbow is presented below:

Median nerve at elbow:
– Motor loss: Weak wrist flexion and abduction, loss of thumb abduction and opposition, loss of flexion of index and middle fingers
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm
– Hand deformity: Ulnar deviation of wrist, thenar wasting, papal benediction on flexing fingers

Median nerve at wrist:
– Motor loss: Loss of thumb abduction and opposition, wrist and finger flexion intact (due to intact AIN)
– Sensory loss: Lateral 3 and ½ fingers and nail beds, lateral side of palm (but can be preserved depending upon palmar cutaneous branch)
– Hand deformity: Thenar wasting, no ulnar deviation of wrist or papal benediction (due to intact AIN)

Obstruction of the long circumferential branches of the basilar artery leads to the lateral pontine syndrome. This condition is characterized by several symptoms. Firstly, there is ataxia, which is caused by damage to the cerebral peduncles. Additionally, there is ipsilateral loss of pain and temperature sense on the face, resulting from damage to CN V. Another symptom is ipsilateral paralysis of the upper and lower face, which occurs due to damage to CN VII. Furthermore, vertigo, nystagmus, tinnitus, deafness, and vomiting are present, all of which are caused by damage to CN VIII. Lastly, there is contralateral sensory loss to the body, which is a result of damage to the spinothalamic tracts.

Alteplase (rt-pA) is recommended for the treatment of acute ischaemic stroke in adults if it is administered as soon as possible within 4.5 hours of the onset of stroke symptoms. It is important to exclude intracranial haemorrhage through appropriate imaging techniques before starting the treatment. The initial dose of alteplase is 0.9 mg/kg, with a maximum dose of 90 mg. This dose should be given intravenously over 60 minutes, with the initial 10% administered by intravenous injection and the remainder by intravenous infusion. In the case of a patient weighing 120 kg, the maximum dose of 90 mg should be administered. For more information, please refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old.

Wernicke’s encephalopathy is a condition that is commonly associated with alcohol abuse and other causes of thiamine deficiency. It is characterized by a triad of symptoms, including acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional features may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. Most cases also involve peripheral neuropathy, which typically affects the legs.

The condition is caused by capillary hemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These changes can be visualized using MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will develop Korsakoff psychosis. This condition is characterized by retrograde amnesia (loss of memory for events that occurred before the onset of amnesia), an inability to form new memories, disordered time perception, and confabulation (fabrication of false memories).

Patients suspected of having Wernicke’s encephalopathy should receive parenteral thiamine (such as Pabrinex) for at least 5 days. Oral thiamine should be administered after the parenteral therapy.

It is important to note that in patients with chronic thiamine deficiency, the infusion of glucose-containing intravenous fluids without thiamine can trigger the development of Wernicke’s encephalopathy.

This patient has developed Wernicke’s encephalopathy, a condition that is associated with alcohol abuse and other causes of thiamine deficiency. It is important to note that the infusion of glucose-containing intravenous fluids without thiamine in a patient with chronic thiamine deficiency can trigger Wernicke’s encephalopathy. In this particular case, it seems that this is what has occurred.

Wernicke’s encephalopathy is typically characterized by a triad of symptoms, which include acute confusion, ophthalmoplegia, and ataxia. Additionally, other possible features of this condition may include papilloedema, hearing loss, apathy, dysphagia, memory impairment, and hypothermia. It is also common for peripheral neuropathy, primarily affecting the legs, to occur in the majority of cases.

This condition is characterized by the presence of acute capillary haemorrhages, astrocytosis, and neuronal death in the upper brainstem and diencephalon. These abnormalities can be visualized through MRI scanning, although CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will go on to develop a Korsakoff psychosis. This condition is characterized by retrograde amnesia, an inability to form new memories, disordered time perception, and confabulation.

Patients who are suspected to have Wernicke’s encephalopathy should be promptly treated with parenteral thiamine (such as Pabrinex) for a minimum of 5 days. Following the parenteral therapy, oral thiamine should be administered.