The ulnar nerve provides innervation to several muscles in the hand. These include the palmar interossei, dorsal interossei, medial two lumbricals, and abductor digiti minimi. On the other hand, the median nerve innervates the opponens pollicis, lateral two lumbricals, and flexor pollicis brevis. Lastly, the radial nerve is responsible for innervating the extensor digitorum muscle.

NICE has emphasized that certain symptoms and signs can indicate specific diseases as the underlying cause of a fever. In the case of meningococcal disease, the presence of a rash that does not fade when pressed upon (non-blanching rash) is particularly suggestive, especially if the child appears unwell, the lesions are larger than 2 mm in diameter (purpura), the capillary refill time is 3 seconds or longer, or there is neck stiffness. For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

A patient with central vertigo would typically show a normal head impulse test result, indicating a normal vestibulo-ocular reflex. However, they would likely have an abnormal alternate cover test result, with a slight vertical correction, suggesting a central lesion like a stroke. A positive Romberg’s test can identify instability related to vertigo but cannot differentiate between peripheral and central causes. On the other hand, a positive Unterberger’s test indicates labyrinth dysfunction but does not indicate a central cause.

Further Reading:

Vertigo is a symptom characterized by a false sensation of movement, such as spinning or rotation, in the absence of any actual physical movement. It is not a diagnosis itself, but rather a description of the sensation experienced by the individual. Dizziness, on the other hand, refers to a perception of disturbed or impaired spatial orientation without a false sense of motion.

Vertigo can be classified as either peripheral or central. Peripheral vertigo is more common and is caused by problems in the inner ear that affect the labyrinth or vestibular nerve. Examples of peripheral vertigo include BPPV, vestibular neuritis, labyrinthitis, and Meniere’s disease. Central vertigo, on the other hand, is caused by pathology in the brain, such as in the brainstem or cerebellum. Examples of central vertigo include migraine, TIA and stroke, cerebellar tumor, acoustic neuroma, and multiple sclerosis.

There are certain features that can help differentiate between peripheral and central vertigo. Peripheral vertigo is often associated with severe nausea and vomiting, hearing loss or tinnitus, and a positive head impulse test. Central vertigo may be characterized by prolonged and severe vertigo, new-onset headache, recent trauma, cardiovascular risk factors, inability to stand or walk with eyes open, focal neurological deficit, and a negative head impulse test.

Nystagmus, an involuntary eye movement, can also provide clues about the underlying cause of vertigo. Central causes of vertigo often have nystagmus that is direction-changing on lateral gaze, purely vertical or torsional, not suppressed by visual fixation, non-fatigable, and commonly large amplitude. Peripheral causes of vertigo often have horizontal nystagmus with a torsional component that does not change direction with gaze, disappears with fixation of the gaze, and may have large amplitude early in the course of Meniere’s disease or vestibular neuritis.

There are various causes of vertigo, including viral labyrinthitis, vestibular neuritis, benign paroxysmal positional vertigo, Meniere’s disease, vertebrobasilar ischemia, and acoustic neuroma. Each of these disorders has its own unique characteristics and may be associated with other symptoms such as hearing loss, tinnitus, or neurological deficits.

When assessing a patient with vertigo, it is important to perform a cardiovascular and neurological examination, including assessing cranial nerves, cerebellar signs, eye movements, gait, coordination, and evidence of peripheral neuropathy.

Dementia with Lewy bodies (DLB) is characterized by several key features, including spontaneous fluctuations in cognitive abilities, visual hallucinations, and Parkinsonism. Visual hallucinations are particularly prevalent in DLB and Parkinson’s disease dementia, which are considered to be part of the same spectrum. While visual hallucinations can occur in other forms of dementia, they are less frequently observed.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or the occurrence of recurrent seizures (2 or more) without any intervening period of neurological recovery.

In the management of a patient with status epilepticus, if the patient has already received two doses of benzodiazepine and is still experiencing seizures, the next step should be to initiate a phenytoin infusion. This involves administering a dose of 15-18 mg/kg at a rate of 50 mg/minute. Alternatively, fosphenytoin can be used as an alternative, and a phenobarbital bolus of 10-15 mg/kg at a rate of 100 mg/minute can also be considered. It is important to note that there is no indication for the administration of intravenous glucose or thiamine in this situation.

The management of status epilepticus involves several general measures. In the early stage (0-10 minutes), the airway should be secured and resuscitation should be performed. Oxygen should be administered and the patient’s cardiorespiratory function should be assessed. Intravenous access should also be established.

In the second stage (0-30 minutes), regular monitoring should be instituted. It is important to consider the possibility of non-epileptic status and commence emergency antiepileptic drug (AED) therapy. Emergency investigations should be conducted, including the administration of glucose (50 ml of 50% solution) and/or intravenous thiamine if there is any suggestion of alcohol abuse or impaired nutrition. Acidosis should be treated if it is severe.

In the third stage (0-60 minutes), the underlying cause of the status epilepticus should be identified. The anaesthetist and intensive care unit (ITU) should be alerted, and any medical complications should be identified and treated. Pressor therapy may be appropriate in certain cases.

In the fourth stage (30-90 minutes), the patient should be transferred to the intensive care unit. Intensive care and EEG monitoring should be established, and intracranial pressure monitoring may be necessary in certain cases. Initial long-term, maintenance AED therapy should also be initiated.

Emergency investigations should include blood tests for blood gases, glucose, renal and liver function, calcium and magnesium, full blood count (including platelets), blood clotting, and AED drug levels.

Erb’s palsy, also known as Erb-Duchenne palsy, is a condition where the arm becomes paralyzed due to an injury to the upper roots of the brachial plexus. The primary root affected is usually C5, although C6 may also be involved in some cases. The main cause of Erb’s palsy is when the arm experiences excessive force during a difficult childbirth, but it can also occur in adults as a result of shoulder trauma.

Clinically, the affected arm will hang by the side with the elbow extended and the forearm turned inward (known as the waiter’s tip sign). Upon examination, there will be a loss of certain movements:

– Shoulder abduction (involving the deltoid and supraspinatus muscles)
– Shoulder external rotation (infraspinatus muscle)
– Elbow flexion (biceps and brachialis muscles)

It is important to differentiate Erb’s palsy from Klumpke’s palsy, which affects the lower roots of the brachial plexus (C8 and T1). Klumpke’s palsy presents with a claw hand due to paralysis of the intrinsic hand muscles, along with sensory loss along the ulnar side of the forearm and hand. If T1 is affected, there may also be the presence of Horner’s syndrome.

In the UK, not all dementia cases are suitable for treatment with acetylcholinesterase inhibitors and memantine. Specifically, patients with frontotemporal dementia should not be prescribed these medications. If a patient experiences visual hallucinations, it may indicate that they have dementia with Lewy bodies.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

The parietal lobes can be divided into two functional areas. One area is responsible for sensation and perception, while the other integrates sensory input primarily from the visual pathways. These lobes play a crucial role in cognition and spatial awareness.

Typically, the left parietal lobe is dominant, and if there are lesions in this area, it can lead to a condition known as Gerstmann’s Syndrome. This syndrome encompasses several difficulties, including problems with writing (agraphia or dysgraphia), arithmetic (acalculia or dyscalculia), and identifying fingers (finger agnosia). Additionally, individuals may experience left-right disorientation and some form of aphasia or dysphasia, affecting their ability to express themselves or understand others.

On the other hand, lesions in the right parietal lobe, which is the non-dominant side, can result in neglecting a part of the body. This can make tasks like dressing and washing challenging.

Parkinson’s disease is often accompanied by two prevalent diseases, namely dementia and depression. Dementia is observed in approximately 20 to 40% of individuals diagnosed with Parkinson’s disease. On the other hand, depression is experienced by around 45% of patients with Parkinson’s disease.

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 anterior interosseous nerve (AIN) and the palmar cutaneous branch. The AIN supplies the flexor pollicis longus, pronator quadratus, and the lateral half of the flexor digitorum profundus. On the other hand, the palmar cutaneous branch 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 remains functional in carpal tunnel syndrome as it travels superficial to the flexor retinaculum. However, it can be damaged by laceration at the wrist.

A comparison of median nerve lesions at the wrist and elbow is presented in the table 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)

Between 60 and 80% of individuals who experience seizures will have their seizure stopped by a single dose of intravenous benzodiazepine. Benzodiazepines have a high solubility in lipids and can quickly pass through the blood-brain barrier. This is why they have a fast onset of action.

As the initial treatment, intravenous lorazepam should be administered. If intravenous lorazepam is not accessible, intravenous diazepam can be used instead. In cases where it is not possible to establish intravenous access promptly, buccal midazolam can be utilized.

Motor Neuron Disease (MND) is a group of degenerative diseases that primarily involve the loss of specific neurons in the motor cortex, cranial nerve nuclei, and anterior horn cells. Both upper and lower motor neurons are affected in this condition. It is important to note that MND does not cause any sensory or sphincter disturbances, and it does not affect eye movements.

MND is relatively uncommon, with a prevalence of approximately 5-7 cases per 100,000 individuals. The median age of onset in the United Kingdom is 60 years, and unfortunately, it often leads to fatality within 2 to 4 years of diagnosis. The treatment for MND mainly focuses on providing supportive care through a multidisciplinary approach.

There are four distinct clinical patterns observed in MND. The first pattern, known as Amyotrophic Lateral Sclerosis (ALS), accounts for up to 50% of MND cases. It involves the loss of motor neurons in both the motor cortex and the anterior horn of the spinal cord. Clinically, individuals with ALS experience weakness and exhibit signs of both upper and lower motor neuron involvement.

The second pattern, called Progressive Bulbar Palsy, occurs in up to 10% of MND cases. This condition specifically affects cranial nerves IX-XII, resulting in Bulbar and pseudobulbar palsy.

Progressive Muscular Atrophy is the third pattern, also seen in up to 10% of MND cases. It primarily affects the anterior horn cells, leading to the presence of only lower motor neuron signs.

Lastly, Primary Lateral Sclerosis involves the loss of Betz cells in the motor cortex. Clinically, individuals with this pattern exhibit upper motor neuron signs, including marked spastic leg weakness and pseudobulbar palsy.

This girl is displaying symptoms and signs that are consistent with a diagnosis of meningococcal septicaemia. It is crucial that she receives urgent antibiotic treatment. If a patient has a penicillin allergy, but not anaphylaxis, a third-generation cephalosporin like cefotaxime may be administered. However, in this particular case, the girl has a documented history of anaphylaxis to penicillin. It is important to note that up to 10% of patients who are allergic to penicillin may experience an adverse reaction to cephalosporins. In situations where there is a true anaphylactic reaction to penicillins, the British National Formulary (BNF) recommends the use of chloramphenicol as an alternative treatment option.

The ulnar nerve originates from the medial cord of the brachial plexus, specifically from the C8-T1 nerve roots. It may also carry fibers from C7 on occasion. This nerve has both motor and sensory functions.

In terms of motor function, the ulnar nerve innervates the muscles of the hand, excluding the thenar muscles and the lateral two lumbricals (which are supplied by the median nerve). It also innervates two muscles in the anterior forearm: the flexor carpi ulnaris and the medial half of the flexor digitorum profundus.

Regarding sensory function, the ulnar nerve provides innervation to the anterior and posterior surfaces of the medial one and a half fingers, as well as the associated palm and dorsal hand area. There are three sensory branches responsible for the cutaneous innervation of the ulnar nerve. Two of these branches arise in the forearm and travel into the hand: the palmar cutaneous branch, which innervates the skin of the medial half of the palm, and the dorsal cutaneous branch, which innervates the dorsal skin of the medial one and a half fingers and the associated dorsal hand. The third branch arises in the hand and is called the superficial branch, which innervates the palmar surface of the medial one and a half fingers.

When the ulnar nerve is damaged at the elbow, the flexor carpi ulnaris and the medial half of the flexor digitorum profundus muscles in the anterior forearm will be spared. However, if the ulnar nerve is injured at the wrist, these muscles will be affected. Additionally, when the ulnar nerve is damaged at the elbow, flexion of the wrist can still occur due to the intact median nerve, but it will be accompanied by abduction as the flexor carpi ulnaris adducts the hand. On the other hand, wrist flexion will be unaffected when the ulnar nerve is damaged at the wrist.

The sensory function also differs depending on the site of damage. When the ulnar nerve is damaged at the elbow, all three cutaneous branches will be affected, resulting in complete sensory loss in the areas innervated by the ulnar nerve. However, if the damage occurs at the wrist, the two branches that arise in the forearm may be spared.

Damage to the ulnar nerve at either the elbow or wrist leads to a characteristic claw hand appearance, characterized by hyperextension of the metacarpophalangeal joints and flexion of the distal and proximal interphalangeal joint of the little and ring fingers.

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 a period of 60 minutes. The first 10% of the dose should be administered through intravenous injection, while the remaining dose should be given through intravenous infusion. For a patient weighing 70 kg, the recommended dose would be 63 mg. For more information, please refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old.

Vomiting after a head injury should raise concerns about increased intracranial pressure (ICP). Signs of elevated ICP include vomiting, changes in pupil size or shape in one eye, decreased cognitive function or consciousness, abnormal findings during fundoscopy (such as blurry optic discs or bleeding in the retina), cranial nerve dysfunction (most commonly affecting CN III and VI), weakness on one side of the body (a late sign), bradycardia (slow heart rate), high blood pressure, and a wide pulse pressure. Irregular breathing that may progress to respiratory distress, focal neurological deficits, and seizures can also be indicative of elevated ICP.

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 intracranial volume refers to the total space inside the skull. The main component of this volume is the brain parenchyma or neural tissue, which makes up the majority of the intracranial volume.

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.

Extradural hematoma is most frequently caused by injury to the middle meningeal artery. This artery is particularly susceptible to damage as it passes behind the pterion.

Further Reading:

Extradural haematoma (EDH) is a collection of blood that forms between the inner surface of the skull and the outer layer of the dura, the dura mater. It is typically caused by head trauma and is often associated with a skull fracture, with the pterion being the most common site of injury. The middle meningeal artery is the most common source of bleeding in EDH.

Clinical features of EDH include a history of head injury with transient loss of consciousness, followed by a lucid interval and gradual loss of consciousness. Other symptoms may include severe headache, sixth cranial nerve palsies, nausea and vomiting, seizures, signs of raised intracranial pressure, and focal neurological deficits.

Imaging of EDH typically shows a biconvex shape and may cause mass effect with brain herniation. It can be differentiated from subdural haematoma by its appearance on imaging.

Management of EDH involves prompt referral to neurosurgery for evacuation of the haematoma. In some cases with a small EDH, conservative management may be considered. With prompt evacuation, the prognosis for EDH is generally good.

Patients with Parkinson’s disease (PD) typically exhibit the following clinical features:

– Hypokinesia (reduced movement)
– Bradykinesia (slow movement)
– Rest tremor (usually occurring at a rate of 4-6 cycles per second)
– Rigidity (increased muscle tone and ‘cogwheel rigidity’)

Other commonly observed clinical features include:

– Gait disturbance (characterized by a shuffling gait and loss of arm swing)
– Loss of facial expression
– Monotonous, slurred speech
– Micrographia (small, cramped handwriting)
– Increased salivation and dribbling
– Difficulty with fine movements

Initially, these signs are typically seen on one side of the body at the time of diagnosis, but they progressively worsen and may eventually affect both sides. In later stages of the disease, additional clinical features may become evident, including:

– Postural instability
– Cognitive impairment
– Orthostatic hypotension

Although PD primarily affects movement, patients often experience psychiatric issues such as depression and dementia. Autonomic disturbances and pain can also occur, leading to significant disability and reduced quality of life for the affected individual. Additionally, family members and caregivers may also be indirectly affected by the disease.

The current algorithm for the treatment of a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, the initial dose of benzodiazepine should be administered. This can be done by giving Lorazepam at a dose of 0.1 mg/kg intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam at a dose of 0.5 mg/kg or rectal diazepam at a dose of 0.5 mg/kg can be given if vascular access is not available.

Step 2 (10 minutes after the start of Step 1):
If the convulsion continues for a further 10 minutes, a second dose of benzodiazepine should be given. It is also important to summon senior help at this point.

Step 3 (10 minutes after the start of Step 2):
At this stage, it is necessary to involve senior help to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already on phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used as an alternative. The recommended dose is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of Step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

Please note that this algorithm is subject to change based on individual patient circumstances and the guidance of medical professionals.

According to the current guidelines from NICE, alteplase is recommended as a thrombolysis treatment for acute ischaemic stroke. For more information, you can refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over the age of 16.

The current algorithm for the treatment of a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, the initial dose of benzodiazepine should be administered. This can be done by giving Lorazepam at a dose of 0.1 mg/kg intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam at a dose of 0.5 mg/kg or rectal diazepam at a dose of 0.5 mg/kg can be given if vascular access is not available.

Step 2 (10 minutes after the start of Step 1):
If the convulsion continues for a further 10 minutes, a second dose of benzodiazepine should be given. It is also important to summon senior help at this point.

Step 3 (10 minutes after the start of Step 2):
At this stage, it is necessary to involve senior help to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already on phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used as an alternative. The recommended dose is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of Step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

Please note that this algorithm is subject to change based on individual patient circumstances and the guidance of medical professionals.

Broca’s area is situated in the frontal lobe of the dominant cerebral hemisphere. Specifically, it can be located in the posterior section of the inferior frontal gyrus, and it comprises of the pars opercularis and the pars triangularis.

Broca’s area is responsible for regulating the motor functions involved in speech production. It facilitates the creation of words through its connections with neighboring motor areas, which stimulate the muscles of the larynx, mouth, tongue, and soft palate.

If there is damage to Broca’s area, it will lead to speech paralysis and expressive aphasia, commonly referred to as Broca’s aphasia.

The NICE recommendations for managing patients with suspected TIA are as follows:

– Offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately.
– Immediately refer individuals who have had a suspected TIA for specialist assessment and investigation. They should be seen within 24 hours of the onset of symptoms.
– Avoid using scoring systems, such as ABCD2, to assess the risk of subsequent stroke or determine the urgency of referral for individuals with suspected or confirmed TIA.
– Provide secondary prevention measures, in addition to aspirin, as soon as possible after confirming the diagnosis of TIA.

The NICE recommendations for imaging in individuals with suspected TIA or acute non-disabling stroke are as follows:

– Do not offer CT brain scanning to individuals with suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect.
– After a specialist assessment in the TIA clinic, consider performing an MRI (including diffusion-weighted and blood-sensitive sequences) to determine the area of ischemia, detect hemorrhage, or identify alternative pathologies. If an MRI is conducted, it should be done on the same day as the assessment.
– Carotid imaging is necessary for all individuals with TIA who, after specialist assessment, are considered candidates for carotid endarterectomy. This imaging should be done urgently.

For more information, refer to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

Intracranial hemorrhages can be categorized based on their location into epidural, subdural, subarachnoid, or intracerebral hemorrhages. The patient in this case is experiencing a severe headache accompanied by signs of meningismus, which strongly suggests a diagnosis of subarachnoid hemorrhage. Additionally, there is no history of trauma, and most cases of subarachnoid hemorrhage are caused by the rupture of a berry aneurysm located in the circle of Willis. Hypertension is a significant risk factor for the rupture of an aneurysm.

During the patient’s hospital stay, they develop an ischemic stroke, which is confirmed by a CT scan. This is most likely a result of cerebral vasospasm secondary to the subarachnoid hemorrhage. To prevent this complication, patients are often treated with the cerebral selective calcium channel blocker Nimodipine.

Another potential complication of this condition is rebleeding, with the highest risk occurring in the first few days. Rebleeding can be potentially fatal, so it is crucial to repair the aneurysm as soon as possible. The presence of blood in the subarachnoid space can also disrupt the production and drainage of cerebrospinal fluid, leading to hydrocephalus.

Long-term complications of subarachnoid hemorrhage include epilepsy, with most patients experiencing their first seizure within a year after the hemorrhage. However, the risk of epilepsy decreases over time. Cognitive dysfunction is also a common long-term complication and can manifest as memory loss, difficulty concentrating, or challenges in performing regular tasks. Emotional problems, such as depression and anxiety, are frequently observed as well.

This patient’s medical history suggests a diagnosis of Guillain-Barré syndrome (GBS). GBS typically presents with initial symptoms of sensory changes or pain, accompanied by muscle weakness in the hands and/or feet. This weakness often spreads to the arms and upper body, affecting both sides. During the acute phase, GBS can be life-threatening, with around 15% of patients experiencing respiratory muscle weakness and requiring mechanical ventilation.

The exact cause of GBS is unknown, but it is believed to involve an autoimmune response where the body’s immune system attacks the myelin sheath surrounding the peripheral nerves. In about 75% of cases, there is a preceding infection, commonly affecting the gastrointestinal or respiratory tracts.

In this particular case, the most likely underlying cause is Campylobacter jejuni, a gastrointestinal pathogen. This is supported by the recent history of a severe diarrheal illness.

This patient presents with a classic case of temporal arteritis, also known as giant cell arteritis (GCA). Temporal arteritis is a chronic condition characterized by inflammation in the walls of medium and large arteries, specifically granulomatous inflammation. It typically affects individuals who are over 50 years old.

The clinical features of temporal arteritis include headache, tenderness in the scalp, jaw claudication, and episodes of sudden blindness or amaurosis fugax (usually occurring in one eye). Some patients may also experience systemic symptoms such as fever, fatigue, loss of appetite, weight loss, and depression.

Temporal arteritis is often associated with polymyalgia rheumatica (PMR) in about 50% of cases. PMR is characterized by stiffness, aching, and tenderness in the upper arms (bilateral) and pain in the pelvic girdle.

Visual loss is an early and significant complication of temporal arteritis, and once it occurs, it rarely improves. Therefore, early treatment with high-dose corticosteroids is crucial to prevent further visual loss and other ischemic complications. If temporal arteritis is suspected, immediate initiation of high-dose glucocorticosteroid treatment (40 – 60 mg prednisolone daily) is necessary. It is also important to arrange an urgent referral for specialist evaluation, including a same-day ophthalmology assessment for those with visual symptoms, and a temporal artery biopsy.

Radial nerve injuries often occur in conjunction with fractures of the humerus. The most common cause of a radial nerve palsy is external compression or trauma to the radial nerve as it passes through the spiral groove in the middle of the humerus.

There are several factors that can lead to damage of the radial nerve in the spiral groove. These include trauma, such as a fracture in the middle of the humerus, compression known as Saturday night palsy, and iatrogenic causes like injections.

When the radial nerve is injured within the spiral groove, it results in weakness of the wrist and metacarpophalangeal joints. However, elbow extension is not affected because the branches to the triceps and anconeus muscles originate before the spiral groove. The interphalangeal joints remain unaffected as well, as they are supplied by the median and ulnar nerves. Sensory loss will be experienced over the dorsal aspect of the forearm, extending from below the elbow to the 1st dorsal interosseous.

In contrast, injury to the radial nerve in the axilla will also cause weakness of elbow extension and sensory loss in the distribution of the more proximal cutaneous branches. This helps distinguish it from injury in the spiral groove.

In the forearm, the posterior interosseous branch of the radial nerve can also be damaged. This can occur due to injury to the radial head or entrapment in the supinator muscle under the arcade of Frohse. However, this type of injury can be easily distinguished from injury in the spiral groove because there is no sensory involvement and no wrist drop, thanks to the preservation of the extensor carpi radialis longus. Nonetheless, there will still be weakness in the wrist and fingers.

Subfalcine herniation occurs when a mass in one side of the brain causes the cingulate gyrus to be pushed under the falx cerebri. This condition often leads to specific neurological symptoms. These symptoms include a motor deficit in the lower limb on the opposite side of the body, bladder incontinence, motor and sensory deficits on the same side of the body as the herniation, and difficulty with speech (dysarthria).

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 posterior interosseous nerve (PIN) is a motor branch of the radial nerve that is located deep within the body. It emerges above the elbow, between the brachioradialis and brachialis muscles, and then divides into two branches: the superficial radial nerve and the PIN. This division occurs at the lateral epicondyle level. As it travels through the forearm, the PIN passes through the supinator muscle, moving from the front to the back surface. In about 30% of individuals, it also passes through a fibrotendinous structure called the arcade of Frohse, which is located below the supinator muscle. The PIN is responsible for supplying all of the extrinsic wrist extensors, with the exception of the extensor carpi radialis longus muscle.

There are several potential causes of damage to the PIN. Fractures, such as a Monteggia fracture, can lead to injury. Inflammation of the radiocapitellar joint, known as radiocapitellar joint synovitis, can also be a contributing factor. Tumors, such as lipomas, may cause damage as well. Additionally, entrapment of the PIN within the arcade of Frohse can result in a condition known as PIN syndrome.

It is important to note that injury to the PIN can be easily distinguished from injury to the radial nerve in other areas of the arm, such as the spiral groove. This is because there will be no sensory involvement and no wrist drop, as the extensor carpi radialis longus muscle remains unaffected.

The anterior interosseous nerve (AIN) is a branch of the median nerve. It primarily functions as a motor nerve, supplying the flexor pollicis longus muscle, the lateral half of the flexor digitorum profundus muscle, and the pronator quadratus muscle. Damage to the AIN can result in weakness and difficulty moving the index and middle fingers.

This woman is displaying symptoms and signs that are in line with a diagnosis of meningococcal septicaemia. In the United Kingdom, the majority of cases of meningococcal septicaemia are caused by Neisseria meningitidis group B.

The implementation of a vaccination program for Neisseria meningitidis group C has significantly reduced the prevalence of this particular type. However, a vaccine for group B disease is currently undergoing clinical trials and is not yet accessible for widespread use.

Co-beneldopa, such as Madopar®, is a medication that combines levodopa and benserazide, a dopa-decarboxylase inhibitor. Levodopa is a precursor of dopamine and has been the primary treatment for Parkinson’s disease since the 1970s. To minimize the side effects of levodopa, it is administered with a dopa-decarboxylase inhibitor (DDI) to reduce its availability in the peripheral system. However, patients may still experience adverse effects like nausea, dizziness, sleepiness, dyskinesia, mood changes, confusion, hallucinations, and delusions.

None of the other combination medications mentioned in this question cause the listed side effects.

Co-dydramol is a pain reliever that contains dihydrocodeine tartrate and paracetamol.

Co-flumactone is a medication that combines spironolactone, a potassium-sparing diuretic, and hydroflumethiazide, a type of thiazide diuretic used for managing congestive cardiac failure.

Co-tenidone is a combination of atenolol and chlorthalidone, primarily used for treating hypertension.

Co-simalcite, also known as Altacite plus, is an antacid that contains two main ingredients: hydrotalcite and activated dimeticone.

Wernicke’s area is situated in the dominant cerebral hemisphere temporal lobe. Specifically, it can be found in the posterior section of the superior temporal gyrus.

This area is responsible for comprehending both written and spoken language. It allows individuals to read a sentence, understand its meaning, and articulate it verbally.

When Wernicke’s area is damaged, patients may be able to string words together fluently, but the resulting phrases lack coherence and meaning. This condition is known as receptive aphasia or Wernicke’s aphasia.

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 temporal lobes play a crucial role in various functions such as processing visual and auditory information, storing memories, and helping us categorize objects. However, if this area of the brain is affected by a stroke, a space-occupying lesion, or trauma, it can lead to several issues. These include problems with understanding and producing language (known as receptive dysphasia), difficulty recognizing faces (prosopagnosia), an inability to categorize objects, difficulty understanding auditory information (auditory agnosia), and impaired perception of music.

The current algorithm for the treatment of a convulsing child, known as APLS, is as follows:

Step 1 (5 minutes after the start of convulsion):
If a child has been convulsing for 5 minutes or more, the initial dose of benzodiazepine should be administered. This can be done by giving Lorazepam at a dose of 0.1 mg/kg intravenously (IV) or intraosseously (IO) if vascular access is available. Alternatively, buccal midazolam at a dose of 0.5 mg/kg or rectal diazepam at a dose of 0.5 mg/kg can be given if vascular access is not available.

Step 2 (10 minutes after the start of Step 1):
If the convulsion continues for a further 10 minutes, a second dose of benzodiazepine should be given. It is also important to summon senior help at this point.

Step 3 (10 minutes after the start of Step 2):
At this stage, it is necessary to involve senior help to reassess the child and provide guidance on further management. The recommended approach is as follows:
– If the child is not already on phenytoin, a phenytoin infusion should be initiated. This involves administering 20 mg/kg of phenytoin intravenously over a period of 20 minutes.
– If the child is already taking phenytoin, phenobarbitone can be used as an alternative. The recommended dose is 20 mg/kg administered intravenously over 20 minutes.
– In the meantime, rectal paraldehyde can be considered at a dose of 0.8 ml/kg of the 50:50 mixture while preparing the infusion.

Step 4 (20 minutes after the start of Step 3):
If the child is still experiencing convulsions at this stage, it is crucial to have an anaesthetist present. A rapid sequence induction with thiopental is recommended for further management.

Please note that this algorithm is subject to change based on individual patient circumstances and the guidance of medical professionals.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this case, the patient has already received two doses of benzodiazepine and is currently on a phenytoin infusion. However, despite these treatments, the seizures persist, and it has been 20 minutes since the infusion started. At this point, the preferred treatment option is to induce general anesthesia. The induction agents that can be considered include thiopental sodium, propofol, and midazolam. There is no need to administer intravenous thiamine in this situation.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose or intravenous thiamine if alcohol abuse or impaired nutrition is suspected
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy if necessary

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate long-term maintenance AED therapy
– Perform further investigations as needed, such as brain imaging or lumbar puncture

Emergency investigations include blood tests for gases, glucose, renal and liver function, calcium and magnesium levels, full blood count (including platelets), blood clotting, and AED drug levels. Serum and urine samples should be saved for future analysis, including toxicology if the cause of convulsive status epilepticus is uncertain. A chest radiograph may be done to evaluate the possibility of aspiration. Additional investigations depend on the clinical circumstances and may include brain imaging or lumbar puncture.

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature.

NICE has emphasized that there are particular symptoms and signs that may indicate specific diseases as the underlying cause of a fever. For instance, bacterial meningitis may be suggested if the following symptoms and signs are present: neck stiffness, bulging fontanelle, decreased level of consciousness, and convulsive status epilepticus. For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Dementia is a condition characterized by a decline in cognitive abilities, such as memory, thinking, and reasoning, that is severe enough to interfere with daily functioning. There are several different causes of dementia, but the leading cause is Alzheimer’s disease. Alzheimer’s disease is a progressive brain disorder that affects memory, thinking, and behavior. It is the most common cause of dementia, accounting for approximately 60-80% of cases.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

Alzheimer’s disease, the leading cause of dementia, is characterized by the presence of beta-amyloid plaques and neurofibrillary tangles in the brain. These plaques are formed due to an excessive buildup of amyloid, which can be caused by either overproduction or impaired clearance of beta-amyloid. The accumulation of amyloid plaques leads to inflammation in the surrounding brain tissue, resulting in damage to neurons. Additionally, the abnormal phosphorylation of tau protein causes it to aggregate into neurofibrillary tangles within neurons. It is important to note that Lewy bodies, composed mainly of alpha-synuclein, are associated with diseases like Parkinson’s disease and dementia with Lewy bodies. Autoimmune diseases often involve the activation of autoreactive T-cells.

Further Reading:

Dementia is a progressive and irreversible clinical syndrome characterized by cognitive and behavioral symptoms. These symptoms include memory loss, impaired reasoning and communication, personality changes, and reduced ability to carry out daily activities. The decline in cognition affects multiple domains of intellectual functioning and is not solely due to normal aging.

To diagnose dementia, a person must have impairment in at least two cognitive domains that significantly impact their daily activities. This impairment cannot be explained by delirium or other major psychiatric disorders. Early-onset dementia refers to dementia that develops before the age of 65.

The most common cause of dementia is Alzheimer’s disease, accounting for 50-75% of cases. Other causes include vascular dementia, dementia with Lewy bodies, and frontotemporal dementia. Less common causes include Parkinson’s disease dementia, Huntington’s disease, prion disease, and metabolic and endocrine disorders.

There are several risk factors for dementia, including age, mild cognitive impairment, genetic predisposition, excess alcohol intake, head injury, depression, learning difficulties, diabetes, obesity, hypertension, smoking, Parkinson’s disease, low social engagement, low physical activity, low educational attainment, hearing impairment, and air pollution.

Assessment of dementia involves taking a history from the patient and ideally a family member or close friend. The person’s current level of cognition and functional capabilities should be compared to their baseline level. Physical examination, blood tests, and cognitive assessment tools can also aid in the diagnosis.

Differential diagnosis for dementia includes normal age-related memory changes, mild cognitive impairment, depression, delirium, vitamin deficiencies, hypothyroidism, adverse drug effects, normal pressure hydrocephalus, and sensory deficits.

Management of dementia involves a multi-disciplinary approach that includes non-pharmacological and pharmacological measures. Non-pharmacological interventions may include driving assessment, modifiable risk factor management, and non-pharmacological therapies to promote cognition and independence. Drug treatments for dementia should be initiated by specialists and may include acetylcholinesterase inhibitors, memantine, and antipsychotics in certain cases.

In summary, dementia is a progressive and irreversible syndrome characterized by cognitive and behavioral symptoms. It has various causes and risk factors, and its management involves a multi-disciplinary approach.

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.

Migraine without aura typically needs to meet the specific criteria set by the International Headache Society. These criteria include experiencing at least five attacks that meet the requirements outlined in criteria 2-4. The duration of these headache attacks should last between 4 to 72 hours. Additionally, the headache should exhibit at least two of the following characteristics: unilateral location, pulsating quality, moderate or severe pain intensity, and aggravation or avoidance of routine physical activity. Furthermore, during the headache, individuals should experience at least one of the following symptoms: nausea and/or vomiting, photophobia, and phonophobia. For more detailed information, you can refer to the guidelines provided by The British Association for the Study of Headache.

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.

Multiple sclerosis is a condition characterized by the demyelination of nerve cells in the brain and spinal cord. It is an autoimmune disease mediated by cells and is caused by recurring inflammation. Typically, it presents in early adulthood, with a female to male ratio of 3:2.

There are several risk factors associated with multiple sclerosis, including being of Caucasian race, living at a greater distance from the equator (as the risk tends to be higher), having a family history of the disease (with 20% of MS patients having an affected relative), and smoking. Interestingly, the rates of relapse tend to decrease during pregnancy.

There are three main patterns of multiple sclerosis. The most common is relapsing and remitting MS, which is characterized by periods of no symptoms followed by relapses (this is seen in 80% of patients at the time of diagnosis). Another pattern is primary progressive MS, where symptoms develop and worsen from the beginning with few remissions (seen in 10-15% of patients at diagnosis). Lastly, there is secondary progressive MS, which occurs after relapsing/remitting MS. In this pattern, symptoms worsen with fewer remissions, and approximately 50% of those with relapsing/remitting MS will develop this within 10 years of diagnosis.

The key to diagnosing MS lies in the history of neurological symptoms that are discrete in time and location of the affected body. Patients often experience fatigue and low mood, particularly during a relapse.

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.

Febrile convulsions are harmless, generalized seizures that occur in otherwise healthy children who have a fever due to an infection outside the brain. To diagnose febrile convulsions, the child must be developing normally, the seizure should last less than 20 minutes, have no complex features, and not cause any lasting abnormalities.

The prognosis for febrile convulsions is generally positive. There is a 30 to 50% chance of experiencing recurrent febrile convulsions, with a 10% risk of recurrence within the first 24 hours. The likelihood of developing long-term epilepsy is around 6%.

Complex febrile convulsions are characterized by certain factors. These include focal seizures, seizures lasting longer than 15 minutes, experiencing more than one convulsion during a single fever episode, or the child being left with a focal neurological deficit.

Overall, febrile convulsions are typically harmless and do not cause any lasting damage.

The cerebellum, also known as the ‘little brain’ in Latin, is a structure within the central nervous system. It is situated at the posterior part of the brain, beneath the occipital and temporal lobes of the cerebral cortex. Despite its relatively small size, the cerebellum houses more than half of the total number of neurons in the brain, accounting for about 10% of its volume.

The cerebellum serves several crucial functions. It is responsible for maintaining balance and posture, ensuring that we stay upright and steady. Additionally, it plays a vital role in coordinating voluntary movements, allowing us to perform tasks that require precise and synchronized actions. The cerebellum is also involved in motor learning, enabling us to acquire new skills and improve our motor abilities over time. Furthermore, it contributes to cognitive function, supporting various mental processes.

It is important to note that spontaneous facial expression is controlled by the frontal lobes and is unlikely to be impacted by a tumor located in the cerebellum.

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.

Carpal tunnel syndrome is a condition where the median nerve becomes trapped, resulting in nerve damage. This can lead to weakness and abnormal sensations in the areas supplied by the median nerve. To remember the muscles that are innervated by the median nerve, you can use the acronym ‘LOAF’: L for the lateral two lumbricals, O for the Opponens pollicis, A for the Abductor pollicis, and F for the Flexor pollicis brevis. It’s important to note that the abductor digiti minimi is not affected by carpal tunnel syndrome as it is innervated by the deep branch of the ulnar nerve.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In this particular patient’s case, his history of chronic alcohol abuse, homelessness, and likely impaired nutrition necessitates the administration of intravenous thiamine in the form of Pabrinex. Additionally, a second dose of benzodiazepine should be given, and his blood glucose levels should be urgently checked.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Implement regular monitoring
– Consider the possibility of non-epileptic status
– Initiate emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose (50 ml of 50% solution) and/or intravenous thiamine as Pabrinex if there are indications of alcohol abuse or impaired nutrition
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Notify the anaesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy when appropriate

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate intracranial pressure monitoring if necessary
– Start initial long-term, maintenance AED therapy

Emergency investigations include blood tests for gases, glucose, renal and liver function, calcium and magnesium levels, full blood count (including platelets), blood clotting, and AED drug levels. Serum and urine samples should be saved for future analysis, including toxicology if the cause of convulsive status epilepticus is uncertain. A chest radiograph may be performed to evaluate the possibility of aspiration. Additional investigations, such as brain imaging or lumbar puncture, depend on the clinical circumstances.

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature.

Guillain-Barré syndrome (GBS) affects approximately 1-2 individuals per 100,000 annually and is a condition that primarily affects the peripheral nervous system, including the autonomic system. The most common initial symptom is weakness in the hands or feet, often accompanied by pain and tingling sensations as the paralysis spreads. Miller Fisher syndrome, a variant of GBS, is characterized by a triad of symptoms: ataxia, areflexia, and ophthalmoplegia.

Due to the potential serious consequences of autonomic involvement, such as fluctuations in blood pressure and cardiac arrhythmias, patients with GBS are typically hospitalized. As the diaphragm becomes paralyzed and swallowing becomes difficult, patients may require ventilation and nasogastric feeding.

GBS is an autoimmune disease that usually develops within three weeks of an infection. The leading cause is Campylobacter jejuni, followed by Epstein-Barr virus, cytomegalovirus, and Mycoplasma pneumoniae. While the patient’s immune response effectively targets the initial infection, it also mistakenly attacks the host tissue.

Symptoms of GBS typically peak around four weeks and then gradually improve. Diagnosis is based on clinical examination, which confirms the presence of areflexia and progressive weakness in the legs (and sometimes arms). Nerve conduction studies and lumbar puncture can also aid in diagnosis, with the latter often showing elevated protein levels and few white blood cells.

Treatment for GBS is primarily supportive, with the use of immunoglobulins to shorten the duration of the illness being common. Plasma exchange may also be utilized, although it has become less common since the introduction of immunoglobulin therapy.

Approximately 80% of patients with GBS make a full recovery, although this often requires a lengthy hospital stay. The mortality rate is around 5%, depending on the availability of necessary facilities such as ventilatory support during the acute phase. Additionally, about 15% of patients may experience some permanent disability, such as weakness or pain.

The Parkinson-plus syndromes are a group of neurodegenerative disorders that share similar features with Parkinson’s disease but also have additional clinical characteristics that set them apart from idiopathic Parkinson’s disease (iPD). These syndromes include Multiple System Atrophy (MSA), Progressive Supranuclear Palsy (PSP), Corticobasal degeneration (CBD), and Dementia with Lewy Bodies (DLB).

Multiple System Atrophy (MSA) is a less common condition than iPD and PSP. It is characterized by the loss of cells in multiple areas of the nervous system. MSA progresses rapidly, often leading to wheelchair dependence within 3-4 years of diagnosis. Some distinguishing features of MSA include autonomic dysfunction, bladder control problems, erectile dysfunction, blood pressure changes, early-onset balance problems, neck or facial dystonia, and a high-pitched voice.

To summarize the distinguishing features of the Parkinson-plus syndromes compared to iPD, the following table provides a comparison:

iPD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Typically starts at rest on one side of the body
– Levodopa response: Excellent response
– Mental changes: Depression
– Balance/falls: Late in the disease
– Common eye abnormalities: Dry eyes, trouble focusing

MSA:
– Symptom onset: Both sides equally affected
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

PSP:
– Symptom onset: Both sides equally affected
– Tremor: Less common, if present affects both sides
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Personality changes, depression
– Balance/falls: Within 1 year
– Common eye abnormalities: Dry eyes, difficulty in looking downwards

CBD:
– Symptom onset: One side of the body affected more than the other
– Tremor: Not common but may occur
– Levodopa response: Minimal response (but often tried in early stages of disease)
– Mental changes: Depression
– Balance/falls: Within 1-3 years
– Common eye abnormalities: Dry eyes, trouble focusing

Febrile convulsions are harmless, generalized seizures that occur in otherwise healthy children who have a fever due to an infection outside the brain. To diagnose febrile convulsions, the child must be developing normally, the seizure should last less than 20 minutes, have no complex features, and not cause any lasting abnormalities.

The prognosis for febrile convulsions is generally positive. There is a 30 to 50% chance of experiencing recurrent febrile convulsions, with a 10% risk of recurrence within the first 24 hours. The likelihood of developing long-term epilepsy is around 6%.

Complex febrile convulsions are characterized by certain factors. These include focal seizures, seizures lasting longer than 15 minutes, experiencing more than one convulsion during a single fever episode, or the child being left with a focal neurological deficit.

Overall, febrile convulsions are typically harmless and do not cause any lasting damage.

Patients who have experienced a stroke should be aware that they are not allowed to drive for at least one month if they have a type 1 license. If there are no neurological issues after this time period, they may not need to inform the DVLA (Driver and Vehicle Licensing Agency). However, they must inform the DVLA if any of the following conditions apply: they have had more than one stroke or transient ischemic attack (TIA), they have a Group 2 license, a medical practitioner has expressed concerns about their ability to drive, they still have residual deficits one month after the stroke (such as weakness in the limbs, visual problems, coordination difficulties, memory or understanding issues), the stroke required neurosurgical treatment, or if they experienced a seizure (unless it was an isolated seizure within 24 hours of the stroke and there is no history of prior seizures).

Further Reading:

Blackouts are a common occurrence in the emergency department and can have serious consequences if they happen while a person is driving. It is crucial for doctors in the ED to be familiar with the guidelines set by the DVLA (Driver and Vehicle Licensing Agency) regarding driving restrictions for patients who have experienced a blackout.

The DVLA has specific rules for different types of conditions that may cause syncope (loss of consciousness). For group 1 license holders (car/motorcycle use), if a person has had a first unprovoked isolated seizure, they must refrain from driving for 6 months or 12 months if there is an underlying causative factor that may increase the risk. They must also notify the DVLA. For group 2 license holders (bus and heavy goods vehicles), the restrictions are more stringent, with a requirement of 12 months off driving for a first unprovoked isolated seizure and 5 years off driving if there is an underlying causative factor.

For epilepsy or multiple seizures, both group 1 and group 2 license holders must remain seizure-free for 12 months before their license can be considered. They must also notify the DVLA. In the case of a stroke or isolated transient ischemic attack (TIA), group 1 license holders need to refrain from driving for 1 month, while group 2 license holders must wait for 12 months before being re-licensed subject to medical evaluation. Multiple TIAs require 3 months off driving for both groups.

Isolated vasovagal syncope requires no driving restriction for group 1 license holders, but group 2 license holders must refrain from driving for 3 months. Both groups must notify the DVLA. If syncope is caused by a reversible and treated condition, group 1 license holders need 4 weeks off driving, while group 2 license holders require 3 months. In the case of an isolated syncopal episode with an unknown cause, group 1 license holders must refrain from driving for 6 months, while group 2 license holders will have their license refused or revoked for 12 months.

For patients who continue to drive against medical advice, the GMC (General Medical Council) has provided guidance on how doctors should manage the situation. Doctors should explain to the patient why they are not allowed to drive and inform them of their legal duty to notify the DVLA or DVA (Driver and Vehicle Agency in Northern Ireland). Doctors should also record the advice given to the patient in their medical record

Occlusion of the posterior inferior cerebellar artery leads to the development of lateral medullary syndrome, also known as Wallenberg’s syndrome. This condition is characterized by several distinct symptoms. Firstly, there is a loss of pain and temperature sensation on the opposite side of the body, which occurs due to damage to the spinothalamic tracts. Additionally, there is a loss of pain and temperature sensation on the same side of the face, resulting from damage to the fifth cranial nerve (CN V).

Furthermore, individuals with lateral medullary syndrome may experience vertigo, nystagmus, tinnitus, deafness, and vomiting. These symptoms arise from damage to the eighth cranial nerve (CN VIII). Lastly, the syndrome may also present with Horner’s syndrome, which is caused by damage to the descending hypothalamospinal tract.

In summary, occlusion of the posterior inferior cerebellar artery causes lateral medullary syndrome, leading to a combination of symptoms including sensory loss, vertigo, tinnitus, and Horner’s syndrome.

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.

Wernicke’s encephalopathy is a condition that is linked to alcohol abuse and other causes of thiamine deficiency. It is commonly identified by the presence of three main symptoms: acute confusion, ophthalmoplegia (paralysis or weakness of the eye muscles), and ataxia (loss of coordination). Additional signs may include papilloedema (swelling of the optic disc), hearing loss, apathy, dysphagia (difficulty swallowing), memory impairment, and hypothermia. Most cases also involve peripheral neuropathy, primarily affecting the legs.

This condition is characterized by the occurrence of acute capillary hemorrhages, astrocytosis (abnormal increase in astrocytes, a type of brain cell), and neuronal death in the upper brainstem and diencephalon. These abnormalities can be detected through MRI scanning, while CT scanning is not very useful for diagnosis.

If left untreated, most patients with Wernicke’s encephalopathy will develop a condition known as 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 perception of time, and confabulation (fabrication of false memories).

When Wernicke’s encephalopathy is suspected, it is crucial to administer parenteral thiamine (such as Pabrinex) for at least 5 days. Following the parenteral therapy, oral thiamine should be continued.

NICE has emphasized that certain indications and manifestations may indicate specific diseases as the underlying cause of fever. For instance, symptoms such as neck stiffness, bulging fontanelle, decreased level of consciousness, and convulsive status epilepticus are suggestive of bacterial meningitis. On the other hand, NICE has identified focal seizures and focal neurological signs as the most indicative of herpes simplex encephalitis. For more information, you can refer to the NICE guidelines on the assessment and initial management of fever in children under 5, as well as the NICE Clinical Knowledge Summary on the management of feverish children.

Alteplase (rt-pA) is a recommended treatment for acute ischaemic stroke in adults if it is initiated within 4.5 hours of the onset of stroke symptoms. It is crucial 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 of 90 mg. This dose is administered intravenously over a period of 60 minutes. The first 10% of the dose is given through intravenous injection, while the remaining amount is administered through intravenous infusion. For more information, please refer to the NICE guidelines on stroke and transient ischaemic attack in individuals aged 16 and above.

If a child who is experiencing convulsions reaches step 3 of the APLS algorithm and has already been given phenytoin as part of their ongoing treatment, it is recommended to initiate a phenobarbitone infusion. This infusion should be administered at a dosage of 20 mg/kg over a period of 30 to 60 minutes.

Status epilepticus is a condition characterized by continuous seizure activity lasting for 5 minutes or more without the return of consciousness, or recurrent seizures (2 or more) without a period of neurological recovery in between. In such cases, the next step in managing the patient would be to administer a second dose of benzodiazepine. Since the patient already has an intravenous line in place, this would be the most appropriate route to choose.

The management of status epilepticus involves several general measures, which are outlined in the following table:

1st stage (Early status, 0-10 minutes):
– Secure the airway and provide resuscitation
– Administer oxygen
– Assess cardiorespiratory function
– Establish intravenous access

2nd stage (0-30 minutes):
– Institute regular monitoring
– Consider the possibility of non-epileptic status
– Start emergency antiepileptic drug (AED) therapy
– Perform emergency investigations
– Administer glucose (50 ml of 50% solution) and/or intravenous thiamine as Pabrinex if there is any suggestion of alcohol abuse or impaired nutrition
– Treat severe acidosis if present

3rd stage (0-60 minutes):
– Determine the underlying cause of status epilepticus
– Alert the anaesthetist and intensive care unit (ITU)
– Identify and treat any medical complications
– Consider pressor therapy when appropriate

4th stage (30-90 minutes):
– Transfer the patient to the intensive care unit
– Establish intensive care and EEG monitoring
– Initiate intracranial pressure monitoring if necessary
– Start initial long-term, maintenance AED therapy

Emergency investigations for status epilepticus include blood tests for gases, glucose, renal and liver function, calcium and magnesium, full blood count (including platelets), blood clotting, and AED drug levels. Serum and urine samples should be saved for future analysis, including toxicology if the cause of the convulsive status epilepticus is uncertain. A chest radiograph may be performed to evaluate the possibility of aspiration. Additional investigations, such as brain imaging or lumbar puncture, depend on the clinical circumstances.

Monitoring during the management of status epilepticus involves regular neurological observations and measurements of pulse, blood pressure, and temperature. ECG, biochemistry, blood gases, clotting, and blood count should also be monitored.

Haloperidol should not be used in patients with Parkinson’s, Lewy body dementia, or prolonged QT syndrome. It is the first choice for controlling aggressive behavior in most patients with delirium, but lorazepam is preferred for patients with Parkinson’s, Lewy body dementia, prolonged QT syndrome, extrapyramidal side effects, or delirium due to alcohol withdrawal. Haloperidol can reduce the effectiveness of levodopa in Parkinson’s disease by blocking dopamine receptors in the corpus striatum, which can lead to worsened motor function, psychosis, or a combination of both.

Further Reading:

Delirium is an acute syndrome that causes disturbances in consciousness, attention, cognition, and perception. It is also known as an acute confusional state. The DSM-IV criteria for diagnosing delirium include recent onset of fluctuating awareness, impairment of memory and attention, and disorganized thinking. Delirium typically develops over hours to days and may be accompanied by behavioral changes, personality changes, and psychotic features. It often occurs in individuals with predisposing factors, such as advanced age or multiple comorbidities, when exposed to new precipitating factors, such as medications or infection. Symptoms of delirium fluctuate throughout the day, with lucid intervals occurring during the day and worse disturbances at night. Falling and loss of appetite are often warning signs of delirium.

Delirium can be classified into three subtypes based on the person’s symptoms. Hyperactive delirium is characterized by inappropriate behavior, hallucinations, and agitation. Restlessness and wandering are common in this subtype. Hypoactive delirium is characterized by lethargy, reduced concentration, and appetite. The person may appear quiet or withdrawn. Mixed delirium presents with signs and symptoms of both hyperactive and hypoactive subtypes.

The exact pathophysiology of delirium is not fully understood, but it is believed to involve multiple mechanisms, including cholinergic deficiency, dopaminergic excess, and inflammation. The cause of delirium is usually multifactorial, with predisposing factors and precipitating factors playing a role. Predisposing factors include older age, cognitive impairment, frailty, significant injuries, and iatrogenic events. Precipitating factors include infection, metabolic or electrolyte disturbances, cardiovascular disorders, respiratory disorders, neurological disorders, endocrine disorders, urological disorders, gastrointestinal disorders, severe uncontrolled pain, alcohol intoxication or withdrawal, medication use, and psychosocial factors.

Delirium is highly prevalent in hospital settings, affecting up to 50% of inpatients aged over 65 and occurring in 30% of people aged over 65 presenting to the emergency department. Complications of delirium include increased risk of death, high in-hospital mortality rates, higher mortality rates following hospital discharge, increased length of stay in hospital, nosocomial infections, increased risk of admission to long-term care or re-admission to hospital, increased incidence of dementia, increased risk of falls and associated injuries and pressure sores.

Hyperventilation leads to the constriction of blood vessels in the brain, which in turn reduces the flow and volume of blood in the brain, ultimately decreasing intracranial pressure (ICP). This is because hyperventilation lowers the levels of carbon dioxide (PaCO2) in the blood, resulting in an increase in pH and causing the arteries in the brain to constrict and reduce blood flow. As a result, cerebral blood volume and ICP decrease. The effects of hyperventilation are immediate, but they gradually diminish over a period of 6-24 hours as the brain adjusts its bicarbonate levels to normalize pH. However, caution must be exercised when discontinuing hyperventilation after a prolonged period, as the sudden increase in PaCO2 can lead to a rapid rise in cerebral blood flow and a detrimental increase in ICP.

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 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.

This patient has been experiencing absence seizures, which are a form of primary generalized epilepsy that is frequently observed in children.

The defining characteristic of absence seizures is a sudden and immediate loss of consciousness, causing a disruption in ongoing activities. During these episodes, individuals may exhibit a vacant stare and occasionally a brief upward movement of the eyes.

While an EEG cannot definitively confirm or rule out an epilepsy diagnosis, it does provide valuable information in the diagnostic process. In the case of absence seizures, EEG results typically reveal generalized spike-and-slow wave complexes occurring at a frequency of 3-4 Hz.

On average, the intracranial volume in adults is around 1400ml.

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.

Henry’s law describes the correlation between the quantity of dissolved gas in a liquid and its partial pressure above the liquid. According to Henry’s law, the amount of gas dissolved in a liquid is directly proportional to the partial pressure of that gas above the liquid. In the case of nitrogen narcosis, as the patient descends deeper into the water, the pressure increases, causing more nitrogen to dissolve in the bloodstream. As the patient ascends, the pressure decreases, leading to a decrease in the amount of dissolved nitrogen and improvement in symptoms.

Further Reading:

Decompression illness (DCI) is a term that encompasses both decompression sickness (DCS) and arterial gas embolism (AGE). When diving underwater, the increasing pressure causes gases to become more soluble and reduces the size of gas bubbles. As a diver ascends, nitrogen can come out of solution and form gas bubbles, leading to decompression sickness or the bends. Boyle’s and Henry’s gas laws help explain the changes in gases during changing pressure.

Henry’s law states that the amount of gas that dissolves in a liquid is proportional to the partial pressure of the gas. Divers often use atmospheres (ATM) as a measure of pressure, with 1 ATM being the pressure at sea level. Boyle’s law states that the volume of gas is inversely proportional to the pressure. As pressure increases, volume decreases.

Decompression sickness occurs when nitrogen comes out of solution as a diver ascends. The evolved gas can physically damage tissue by stretching or tearing it as bubbles expand, or by provoking an inflammatory response. Joints and spinal nervous tissue are commonly affected. Symptoms of primary damage usually appear immediately or soon after a dive, while secondary damage may present hours or days later.

Arterial gas embolism occurs when nitrogen bubbles escape into the arterial circulation and cause distal ischemia. The consequences depend on where the embolism lodges, ranging from tissue ischemia to stroke if it lodges in the cerebral arterial circulation. Mechanisms for distal embolism include pulmonary barotrauma, right to left shunt, and pulmonary filter overload.

Clinical features of decompression illness vary, but symptoms often appear within six hours of a dive. These can include joint pain, neurological symptoms, chest pain or breathing difficulties, rash, vestibular problems, and constitutional symptoms. Factors that increase the risk of DCI include diving at greater depth, longer duration, multiple dives close together, problems with ascent, closed rebreather circuits, flying shortly after diving, exercise shortly after diving, dehydration, and alcohol use.

Diagnosis of DCI is clinical, and investigations depend on the presentation. All patients should receive high flow oxygen, and a low threshold for ordering a chest X-ray should be maintained. Hydration is important, and IV fluids may be necessary. Definitive treatment is recompression therapy in a hyperbaric oxygen chamber, which should be arranged as soon as possible. Entonox should not be given, as it will increase the pressure effect in air spaces.

Parkinson’s disease is primarily characterized by the degeneration of cells in the substantia nigra, a region located in the midbrain. The most severely affected part is the pars compacta, which plays a crucial role in motor control. As a result, there is a significant decrease in the activity of cells that secrete dopamine.

The main symptoms of Parkinson’s disease include tremors that occur when the body is at rest, rigidity in the muscles, and bradykinesia, which refers to a slowness in movement. These symptoms can greatly impact a person’s ability to perform everyday tasks and can progressively worsen over time.

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)

This individual has a typical history for a transient ischaemic attack (TIA). According to the NICE recommendations, it is advised to offer aspirin (300 mg daily) to individuals who have experienced a suspected TIA, unless there are contraindications. This treatment should be started immediately. It is also important to refer individuals who have had a suspected TIA for specialist assessment and investigation, with the aim of being seen within 24 hours of symptom onset. Scoring systems, such as ABCD2, should not be used to assess the risk of subsequent stroke or determine the urgency of referral for individuals with a suspected or confirmed TIA. Secondary prevention measures, in addition to aspirin, should be offered as soon as possible after the diagnosis of TIA is confirmed.

In terms of imaging, it is not recommended to offer CT brain scanning to individuals with a suspected TIA, unless there is clinical suspicion of an alternative diagnosis that CT could detect. After a specialist assessment in the TIA clinic, MRI (including diffusion-weighted and blood-sensitive sequences) may be considered to determine the area of ischaemia, detect haemorrhage, or identify alternative pathologies. If an MRI is performed, it should ideally be done on the same day as the assessment. Carotid imaging is also important for everyone with a TIA who is considered a candidate for carotid endarterectomy, and this should be done urgently.

to the NICE guidelines on stroke and transient ischaemic attack in individuals over 16 years old: diagnosis and initial management.

Due to the potentially life-threatening nature of the disease, it is crucial to initiate treatment without waiting for laboratory confirmation. Immediate administration of antibiotics is necessary.

In a hospital setting, the preferred agents for treatment are IV ceftriaxone (2 g for adults; 80 mg/kg for children) or IV cefotaxime (2 g for adults; 80 mg/kg for children). In the prehospital setting, IM benzylpenicillin can be given as an alternative. If there is a history of anaphylaxis to cephalosporins, chloramphenicol is a suitable alternative.

It is important to prioritize prompt treatment due to the severity of the disease. The recommended antibiotics should be administered as soon as possible to ensure the best possible outcome for the patient.

The most probable diagnosis in this case is idiopathic intracranial hypertension, also known as benign intracranial hypertension or pseudotumour cerebri. This condition typically affects overweight women in their 20s and 30s.

The clinical features of idiopathic intracranial hypertension include:
– Headache: The headache is usually worse in the morning and evenings, relieved by standing, and worsened when lying down. It can also be aggravated by coughing and sneezing. Some patients may experience pain around the shoulder girdle.
– Nausea and vomiting
– Visual field defects: These develop gradually over time.
– 6th nerve palsy and diplopia
– Bilateral papilloedema

To investigate this condition, the patient should undergo a CT scan and/or MRI of the brain, as well as a lumbar puncture to measure the opening pressure and analyze the cerebrospinal fluid (CSF).

The primary treatment goal for idiopathic intracranial hypertension is to prevent visual loss. This can be achieved through one of the following strategies:
– Repeated lumbar puncture to control intracranial pressure (ICP)
– Medical treatment with acetazolamide
– Surgical decompression of the optic nerve sheath

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.

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 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.

This patient’s medical history suggests a diagnosis of Guillain-Barré syndrome (GBS). GBS typically presents with initial symptoms of sensory changes or pain, accompanied by muscle weakness in the hands and/or feet. This weakness often spreads to the arms and upper body, affecting both sides. During the acute phase, GBS can be life-threatening, with around 15% of patients experiencing respiratory muscle weakness and requiring mechanical ventilation.

The exact cause of GBS is unknown, but it is believed to involve an autoimmune response where the body’s immune system attacks the myelin sheath surrounding the peripheral nerves. In about 75% of cases, there is a preceding infection, commonly affecting the gastrointestinal or respiratory tracts.

In this particular case, the most likely underlying cause is Campylobacter jejuni, a gastrointestinal pathogen. This is supported by the recent history of a severe diarrheal illness.

Erb’s palsy, also known as Erb-Duchenne palsy, is a condition where the arm becomes paralyzed due to an injury to the upper roots of the brachial plexus. The primary root affected is usually C5, although C6 may also be involved in some cases. The main cause of Erb’s palsy is when the arm experiences excessive force during a difficult childbirth, but it can also occur in adults as a result of shoulder trauma.

Clinically, the affected arm will hang by the side with the elbow extended and the forearm turned inward (known as the waiter’s tip sign). Upon examination, there will be a loss of certain movements:

– Shoulder abduction (involving the deltoid and supraspinatus muscles)
– Shoulder external rotation (infraspinatus muscle)
– Elbow flexion (biceps and brachialis muscles)

It is important to differentiate Erb’s palsy from Klumpke’s palsy, which affects the lower roots of the brachial plexus (C8 and T1). Klumpke’s palsy presents with a claw hand due to paralysis of the intrinsic hand muscles, along with sensory loss along the ulnar side of the forearm and hand. If T1 is affected, there may also be the presence of Horner’s syndrome.

This patient’s history is indicative of episodic tension-type headache. Chronic tension-type headache is defined as experiencing headaches on more than 15 days per month.

Migraine with typical aura presents with temporary visual disturbances such as hemianopia or scintillating scotoma that spreads. Migraine without aura must meet the criteria set by the International Headache Society, which are outlined below:

1. The patient must have at least five attacks that meet criteria 2-4.
2. The duration of each headache attack should be between 4 and 72 hours.
3. The headache must have at least two of the following characteristics:
– Located on one side of the head
– Pulsating quality
– Moderate or severe pain intensity
– Aggravation or avoidance of routine physical activity (e.g., walking or climbing stairs)
4. During the headache, the patient must experience at least one of the following:
– Nausea and/or vomiting
– Sensitivity to light (photophobia) and sound (phonophobia)
5. The headache should not be attributed to another disorder.

Medication overuse headache is suspected when a patient uses multiple medications, often at low doses, without experiencing any relief from their headaches. Combination medications containing barbiturates, codeine, and caffeine are frequently involved. The diagnosis can only be confirmed when the symptoms improve after discontinuing the medication.