The length of the spinal cord is around 45cm in males and 43cm in females. The denticulate ligament is an extension of the pia mater, which has sporadic lateral projections that connect the spinal cord to the dura mater.

The spinal cord is a central structure located within the vertebral column that provides it with structural support. It extends rostrally to the medulla oblongata of the brain and tapers caudally at the L1-2 level, where it is anchored to the first coccygeal vertebrae by the filum terminale. The cord is characterised by cervico-lumbar enlargements that correspond to the brachial and lumbar plexuses. It is incompletely divided into two symmetrical halves by a dorsal median sulcus and ventral median fissure, with grey matter surrounding a central canal that is continuous with the ventricular system of the CNS. Afferent fibres entering through the dorsal roots usually terminate near their point of entry but may travel for varying distances in Lissauer’s tract. The key point to remember is that the anatomy of the cord will dictate the clinical presentation in cases of injury, which can be caused by trauma, neoplasia, inflammatory diseases, vascular issues, or infection.

One important condition to remember is Brown-Sequard syndrome, which is caused by hemisection of the cord and produces ipsilateral loss of proprioception and upper motor neuron signs, as well as contralateral loss of pain and temperature sensation. Lesions below L1 tend to present with lower motor neuron signs. It is important to keep a clinical perspective in mind when revising CNS anatomy and to understand the ways in which the spinal cord can become injured, as this will help in diagnosing and treating patients with spinal cord injuries.

The proximal tubule is responsible for the reabsorption of phosphate. This patient’s symptoms are consistent with hyperparathyroidism, which causes an increase in serum calcium levels and a decrease in phosphate levels due to increased osteoclast activity, increased renal and intestinal absorption of calcium, and reduced renal reabsorption of phosphate from the proximal tubule. Treatment for primary hyperparathyroidism typically involves a parathyroidectomy, but medical treatment can be used if surgery is not possible.

The distal tubules absorb electrolytes such as sodium, potassium, and calcium, and play a role in pH regulation through the absorption and secretion of bicarbonate and protons. However, only a minimal amount of phosphate is reabsorbed in the distal tubules.

The duodenum and jejunum are responsible for the absorption of iron and folate, respectively, but only a small amount of phosphate is reabsorbed in the gastrointestinal tract as a whole.

The loop of Henle reabsorbs several electrolytes, including sodium, potassium, chloride, magnesium, and calcium, but only a relatively small amount of phosphate is reabsorbed in this aspect of the renal tract.

The terminal ileum absorbs vitamin B12 and bile salts, but again, only a very small amount of phosphate is reabsorbed in the GI tract.

Maintaining Calcium Balance in the Body

Calcium ions are essential for various physiological processes in the body, and the largest store of calcium is found in the skeleton. The levels of calcium in the body are regulated by three hormones: parathyroid hormone (PTH), vitamin D, and calcitonin.

PTH increases calcium levels and decreases phosphate levels by increasing bone resorption and activating osteoclasts. It also stimulates osteoblasts to produce a protein signaling molecule that activates osteoclasts, leading to bone resorption. PTH increases renal tubular reabsorption of calcium and the synthesis of 1,25(OH)2D (active form of vitamin D) in the kidney, which increases bowel absorption of calcium. Additionally, PTH decreases renal phosphate reabsorption.

Vitamin D, specifically the active form 1,25-dihydroxycholecalciferol, increases plasma calcium and plasma phosphate levels. It increases renal tubular reabsorption and gut absorption of calcium, as well as osteoclastic activity. Vitamin D also increases renal phosphate reabsorption in the proximal tubule.

Calcitonin, secreted by C cells of the thyroid, inhibits osteoclast activity and renal tubular absorption of calcium.

Although growth hormone and thyroxine play a small role in calcium metabolism, the primary regulation of calcium levels in the body is through PTH, vitamin D, and calcitonin. Maintaining proper calcium balance is crucial for overall health and well-being.

Normal pressure hydrocephalus can be a reversible cause of dementia, while Pick’s disease is a degenerative form of frontotemporal dementia that cannot be reversed. Lewy body dementia is a progressive condition that is linked to parkinson’s and visual hallucinations. Multi-infarct dementia is associated with cardiovascular risk factors like smoking, diabetes, and atrial fibrillation, but the damage caused by infarcts is irreversible. A brain tumor is a potential cause of dementia that can be reversed.

Understanding the Causes of Dementia

Dementia is a condition that affects millions of people worldwide, and it is caused by a variety of factors. The most common causes of dementia include Alzheimer’s disease, cerebrovascular disease, and Lewy body dementia. These conditions account for around 40-50% of all cases of dementia.

However, there are also rarer causes of dementia, which account for around 5% of cases. These include Huntington’s disease, Creutzfeldt-Jakob disease (CJD), Pick’s disease, and HIV (in 50% of AIDS patients). These conditions are less common but can still have a significant impact on those affected.

It is also important to note that there are several potentially treatable causes of dementia that should be ruled out before a diagnosis is made. These include hypothyroidism, Addison’s disease, B12/folate/thiamine deficiency, syphilis, brain tumours, normal pressure hydrocephalus, subdural haematoma, depression, and chronic drug use (such as alcohol or barbiturates).

In conclusion, understanding the causes of dementia is crucial for effective diagnosis and treatment. While some causes are more common than others, it is important to consider all potential factors and rule out treatable conditions before making a final diagnosis.

Even if there are nerve lesions located proximally, complete loss of triceps muscle function may not occur as the axillary nerve can innervate the long head of the triceps muscle.

The Radial Nerve: Anatomy, Innervation, and Patterns of Damage

The radial nerve is a continuation of the posterior cord of the brachial plexus, with root values ranging from C5 to T1. It travels through the axilla, posterior to the axillary artery, and enters the arm between the brachial artery and the long head of triceps. From there, it spirals around the posterior surface of the humerus in the groove for the radial nerve before piercing the intermuscular septum and descending in front of the lateral epicondyle. At the lateral epicondyle, it divides into a superficial and deep terminal branch, with the deep branch crossing the supinator to become the posterior interosseous nerve.

The radial nerve innervates several muscles, including triceps, anconeus, brachioradialis, and extensor carpi radialis. The posterior interosseous branch innervates supinator, extensor carpi ulnaris, extensor digitorum, and other muscles. Denervation of these muscles can lead to weakness or paralysis, with effects ranging from minor effects on shoulder stability to loss of elbow extension and weakening of supination of prone hand and elbow flexion in mid prone position.

Damage to the radial nerve can result in wrist drop and sensory loss to a small area between the dorsal aspect of the 1st and 2nd metacarpals. Axillary damage can also cause paralysis of triceps. Understanding the anatomy, innervation, and patterns of damage of the radial nerve is important for diagnosing and treating conditions that affect this nerve.

The Moro reflex vanishes by the time the baby reaches 4 months of age.

Primitive Reflexes in Infants

Primitive reflexes are automatic movements that are present in infants from birth to a certain age. These reflexes are important for survival and development in the early stages of life. One of the most well-known primitive reflexes is the Moro reflex, which is triggered by head extension and causes the arms to first spread out and then come back together. This reflex is present from birth to around 3-4 months of age.

Another primitive reflex is the grasp reflex, which causes the fingers to flex when an object is placed in the infant’s palm. This reflex is present from birth to around 4-5 months of age and is important for the infant’s ability to grasp and hold objects.

The rooting reflex is another important primitive reflex that assists in breastfeeding. When the infant’s cheek is touched, they will turn their head towards the touch and open their mouth to suck. This reflex is present from birth to around 4 months of age.

Finally, the stepping reflex, also known as the walking reflex, is present from birth to around 2 months of age. When the infant’s feet touch a flat surface, they will make stepping movements as if they are walking. This reflex is important for the development of the infant’s leg muscles and coordination.

Overall, primitive reflexes are an important part of infant development and can provide insight into the health and functioning of the nervous system.

Neuropraxia typically results in full recovery within 6-8 weeks after nerve injury, and Wallerian degeneration is not a common occurrence. Additionally, autonomic function is typically maintained.

Nerve injuries can be classified into three types: neuropraxia, axonotmesis, and neurotmesis. Neuropraxia occurs when the nerve is intact but its electrical conduction is affected. However, full recovery is possible, and autonomic function is preserved. Wallerian degeneration, which is the degeneration of axons distal to the site of injury, does not occur. Axonotmesis, on the other hand, happens when the axon is damaged, but the myelin sheath is preserved, and the connective tissue framework is not affected. Wallerian degeneration occurs in this type of injury. Lastly, neurotmesis is the most severe type of nerve injury, where there is a disruption of the axon, myelin sheath, and surrounding connective tissue. Wallerian degeneration also occurs in this type of injury.

Wallerian degeneration typically begins 24-36 hours following the injury. Axons are excitable before degeneration occurs, and the myelin sheath degenerates and is phagocytosed by tissue macrophages. Neuronal repair may only occur physiologically where nerves are in direct contact. However, nerve regeneration may be hampered when a large defect is present, and it may not occur at all or result in the formation of a neuroma. If nerve regrowth occurs, it typically happens at a rate of 1mm per day.

Chronic pain is defined by the WHO as pain that lasts for more than 12 weeks. Therefore, the correct answer is 12 weeks, and all other options are incorrect.

Guidelines for Managing Chronic Pain

Chronic pain is defined as pain that lasts for more than 12 weeks and can include conditions such as musculoskeletal pain, neuropathic pain, vascular insufficiency, and degenerative disorders. In 2013, the Scottish Intercollegiate Guidelines Network (SIGN) produced guidelines for the management of chronic, non-cancer related pain.

Non-pharmacological interventions are recommended by SIGN, including self-management information, exercise, manual therapy, and transcutaneous electrical nerve stimulation (TENS). Exercise has been shown to be effective in improving chronic pain, and specific support such as referral to an exercise program is recommended. Manual therapy is particularly effective for spinal pain, while TENS can also be helpful.

Pharmacological interventions may be necessary, but if medications are not effective after 2-4 weeks, they are unlikely to be effective. For neuropathic pain, SIGN recommends gabapentin or amitriptyline as first-line treatments. NICE also recommends pregabalin or duloxetine as first-line treatments. For fibromyalgia, duloxetine or fluoxetine are recommended.

If patients are using more than 180 mg/day morphine equivalent, experiencing significant distress, or rapidly escalating their dose without pain relief, SIGN recommends referring them to specialist pain management services.

Overall, the management of chronic pain requires a comprehensive approach that includes both non-pharmacological and pharmacological interventions, as well as referral to specialist services when necessary.

Anterior cord lesions result in motor deficits because the ventral (anterior) horns of the spinal cord contain motor neuron cell bodies. These motor neurons run along the ventral corticospinal tract, which is responsible for voluntary bodily movement. Therefore, compression of the ventral part of the spinal cord by a tumor may cause paresis or paralysis below the level of the lesion. However, pain and temperature loss below the level of the lesion would be from compression of the spinothalamic tract, which runs more laterally in the spinal cord. Proprioception loss below the level of the lesion is also incorrect as it is neurologically tied to the dorsal-column medial-lemniscus tract, which runs dorsally. Additionally, spinal lesions affect sensory experience below the level of the lesion rather than above.

The spinal cord is a central structure located within the vertebral column that provides it with structural support. It extends rostrally to the medulla oblongata of the brain and tapers caudally at the L1-2 level, where it is anchored to the first coccygeal vertebrae by the filum terminale. The cord is characterised by cervico-lumbar enlargements that correspond to the brachial and lumbar plexuses. It is incompletely divided into two symmetrical halves by a dorsal median sulcus and ventral median fissure, with grey matter surrounding a central canal that is continuous with the ventricular system of the CNS. Afferent fibres entering through the dorsal roots usually terminate near their point of entry but may travel for varying distances in Lissauer’s tract. The key point to remember is that the anatomy of the cord will dictate the clinical presentation in cases of injury, which can be caused by trauma, neoplasia, inflammatory diseases, vascular issues, or infection.

One important condition to remember is Brown-Sequard syndrome, which is caused by hemisection of the cord and produces ipsilateral loss of proprioception and upper motor neuron signs, as well as contralateral loss of pain and temperature sensation. Lesions below L1 tend to present with lower motor neuron signs. It is important to keep a clinical perspective in mind when revising CNS anatomy and to understand the ways in which the spinal cord can become injured, as this will help in diagnosing and treating patients with spinal cord injuries.

The Tibial Nerve: Muscles Innervated and Termination

The tibial nerve is a branch of the sciatic nerve that begins at the upper border of the popliteal fossa. It has root values of L4, L5, S1, S2, and S3. This nerve innervates several muscles, including the popliteus, gastrocnemius, soleus, plantaris, tibialis posterior, flexor hallucis longus, and flexor digitorum brevis. These muscles are responsible for various movements in the lower leg and foot, such as plantar flexion, inversion, and flexion of the toes.

The tibial nerve terminates by dividing into the medial and lateral plantar nerves. These nerves continue to innervate muscles in the foot, such as the abductor hallucis, flexor digitorum brevis, and quadratus plantae. The tibial nerve plays a crucial role in the movement and function of the lower leg and foot, and any damage or injury to this nerve can result in significant impairments in mobility and sensation.

When a patient complains of difficulty with eating, it is crucial to determine whether the issue is related to a problem with swallowing or with the muscles used for chewing.

The correct answer is CN V. This nerve, also known as the trigeminal nerve, controls the muscles involved in chewing. Damage to this nerve, which can occur due to various reasons including stroke, can result in weakness or paralysis of these muscles on the same side of the face. In this case, the patient’s stroke occurred two years ago, and he likely has some wasting of the mastication muscles due to disuse atrophy. As a result, he may have difficulty chewing food, but his ability to swallow is likely unaffected.

The other options are incorrect. CN IV, also known as the trochlear nerve, controls a muscle involved in eye movement and is not involved in eating. CN VII, or the facial nerve, controls facial movements but not the muscles of mastication. Damage to this nerve can result in facial weakness, but it would not affect the ability to chew. CN X, or the vagus nerve, is important for swallowing, but the stem indicates that the patient’s swallow is functional, making it less likely that this nerve is involved in his eating difficulties.

Cranial nerves are a set of 12 nerves that emerge from the brain and control various functions of the head and neck. Each nerve has a specific function, such as smell, sight, eye movement, facial sensation, and tongue movement. Some nerves are sensory, some are motor, and some are both. A useful mnemonic to remember the order of the nerves is Some Say Marry Money But My Brother Says Big Brains Matter Most, with S representing sensory, M representing motor, and B representing both.

In addition to their specific functions, cranial nerves also play a role in various reflexes. These reflexes involve an afferent limb, which carries sensory information to the brain, and an efferent limb, which carries motor information from the brain to the muscles. Examples of cranial nerve reflexes include the corneal reflex, jaw jerk, gag reflex, carotid sinus reflex, pupillary light reflex, and lacrimation reflex. Understanding the functions and reflexes of the cranial nerves is important in diagnosing and treating neurological disorders.