nyuuzyou/wikis huggingface dataset:
Metacarpophalangeal Joint

The metacarpophalangeal joints (MCP) are condyloid joints situated between the metacarpal bones and the proximal phalanges of the fingers. The are formed by the reception of the rounded heads of the metacarpal bones into shallow cavities on the proximal ends of the proximal phalanges. The condyloid formation allows the movements of flexion, extension, abduction, adduction and circumduction.
Arthritis of the MCP is a distinguishing feature of Rheumatoid Arthritis, as opposed to the distal interphalangeal joint in Osteoarthritis.
==Ligaments==
Two collateral ligaments
These strengthen the capsule on each side and pass from the head of the metacarpal to the base of the phalanx.
Palmar ligament (volar ligament)
A fibrocartilaginous plate that connects the collateral ligaments and attaches firmly to the base of the proximal phalanx and loosely to the head of the metacarpal
File:Gray337 Metacarpophalangeal joint and digit palmar.png
File:Gray338 Metacarpophalangeal joint and digit ulnar.png
Category:Hand and Wrist Anatomy
Category:Joints of the Upper Limb
Metatarsophalangeal Joints

The five metatarsophalangeal joints are each composed of a convex metatarsal head and a concave proximal phalanx.
==Motion==
The primary motion is dorsiflexion and plantarflexion, with a lesser amount of abduction and adduction. Passive range of motion is 65° for dorsiflexion, and 40° for plantarflexion for joints 2-5. The first MTPJ has 85° of dorsiflexion
During normal toe-off, the MTPJ needs to dorsiflex to 60°. Other tasks such as sitting on the heels or standing on tiptoes requires greater dorsiflexion. 
There is some tangential sliding of the first MTPJ from maximum plantarflexion to moderate dorsiflexion, along with some compression dorsally at maximum dorsiflexion. With full dorsiflexion the metatarsal head surface contact area shifts dorsally as joint compression occurs. This is the reason for dorsal osteophyte formation and limited dorsiflexion of the proximal phalanx in hallux rigidus.
The windlass mechanism of the plantar aponeurosis provides stability to the medial aspect of the foot with great toe dorsiflexion. The peroneus longus muscle acts to press the metatarsal head into the ground when the body passes over the foot in toe-off.
==Ligaments==
*Medial and lateral collateral ligaments: primary ligaments.
*Four transverse metatarsal ligaments: bind the metatarsal heads together, providing stability for the forefoot.
==Clinical Applications==
Narrow high-heeled shoe wearing can lead to mechanical entrapment of the interdigital nerves, most commonly the third. The nerves are pressed against the transverse intermetatarsal ligaments and metatarsal heads, leading to neuroma formation
First MTPJ stress fractures or inflammation can occur with excessive stress on the joint. Pain can occur in the sesamoid bones which are found within the flexor hallucis brevis tendon.
==References==
*Basic Biomechanics of the Musculoskeletal System - Nordin 4th edition 2012
Category:Foot and Ankle Anatomy
Category:Joints
Category:Joints of the Lower Limb
Migraine

== Management ==
Table 1: Preventive migraine treatment
Drug class 	Drug 	Dosage and route 	Contraindications 	NZ Note
First line medications 	First line medications 	First line medications 	First line medications 	
Beta blockers 	Atenolol 	25–100 mg oral twice daily 	Asthma, cardiac failure, Raynaud disease, atrioventricular block, depression 	
Beta blockers 	Bisoprolol 	5–10 mg oral once daily 	 	
Beta blockers 	Metoprolol 	50–100 mg oral twice daily or 200 mg modified-release oral once daily 	 	
Beta blockers 	Propranolol 	80–160 mg oral once or twice daily in long-acting formulations 	 	Limited range of formulations limits ease of titration. 160mg MR, 10 and 40mg SR.
Angiotensin II-receptor blocker 	Candesartan 	16–32 mg oral per day 	Co-administration of aliskiren 	
Anticonvulsant 	Topiramate 	50–100 mg oral daily 	Nephrolithiasis, pregnancy, lactation, glaucoma 	
Second line medications 	Second line medications	Second line medications 	Second line medications 	
Tricyclic antidepressant 	Amitriptyline 	10–100 mg oral at night 	Age <6 years, heart failure, co-administration with monoamine oxidase inhibitors and SSRIs, glaucoma 	
Calcium antagonist 	Flunarizine 	5–10 mg oral once daily 	Parkinsonism, depression 	Section 29, not funded
Anticonvulsant 	Sodium valproate 	600–1,500 mg oral once daily 	Liver disease, thrombocytopenia, female and of childbearing potential 	
Third line medications 	Third line medications 	Third line medications 	Third line medications 	
Botulinum toxin 	OnabotulinumtoxinA 	155–195 units to 31–39 sites every 12 weeks 	Infection at injection site 	Not funded
Calcitonin gene-related peptide monoclonal antibodies	Erenumab 	70 or 140 mg subcutaneous once monthly 	Hypersensitivity. Not recommended in patients with a history of stroke, subarachnoid haemorrhage, coronary heart disease, inflammatory bowel disease, chronic obstructive pulmonary disease, or impaired wound healing	Not funded
Calcitonin gene-related peptide monoclonal antibodies	Fremanezumab 	225 mg subcutaneous once monthly or 675 mg subcutaneous once quarterly	 	Not available
Calcitonin gene-related peptide monoclonal antibodies	Galcanezumab 	240 mg subcutaneous, then 120 mg subcutaneous once monthly 	 	Not funded
Calcitonin gene-related peptide monoclonal antibodies	Eptinezumab 	100 or 300 mg intravenous quarterly 	 	Not available
==Resources==
== References ==
Category:Headache Disorders
Category:Head and Jaw Conditions
Muscles of the Ankle and Foot

* Strongest plantarflexor - Achilles tendon. 
** Inserts onto the posterior-medial calcaneus. 
** Fires during midstance to slow the forward motion of the tibia over the foot
* Strongest dorsiflexor - tibialis anterior. 
** Provides eccentric control during stance from heel-strike to foot flat. 
** Prevents foot slap, and during swing phase is allows clearance of the foot from the floor
* Strongest inverter - posterior tibialis muscle. 
** Dynamic supporter of the medial longitudinal arch. Inverts the subtalar joint during mid and late stance which results in locking of the transverse tarsal joint providing rigidity to the foot during toe-off. 
** Loss of this muscle results in acquired pes planus. The arch flattens, the forefoot abducts, and the heel everts. The patient is unable to actively invert their heel during toe rise.
* Primary everters - peroneus longus and peroneus brevis. 
** Peroneus longus
*** Inserts on the base of the first metatarsal and medial cuneiform. 
*** Depresses (plantarflexes) the metatarsal head at the tarsometatarsal joint. 
*** Loss of this muscle results in elevation of the first metatarsal head, decreasing loads on the first metatarsal, and results in dorsal bunion development.
** Peroneus brevis - strongest everter 
*** Stabilises the forefoot laterally by resisting inversion.
*** Loss of this muscle results in varus of the hindfoot.
* Interosseus muscles
** Active during late stance, stabilises the forefoot during toe-off.
** Imbalance between intrinsics and extrinsics leads to toe deformities such as hammer toes, claw toes, and mallet toes
* Intrinsic and extrinsic muscles
** Flexor digitorum brevis - primary flexor of the PIPJ
** Flexor digitorum longus - primary flexor of the DIPJ
** Sesamoid bones within flexor hallucis brevis under the head of the first metatarsal increases lever arm distance of the muscle enabling greater flexion torque at the first MTPJ by moving the tendon away from the centre of the joint
** Extrinsic extensors extend the MTPJ through the sagittal bands by lifting the proximal phalanges into extension.
== References ==
* Basic Biomechanics of the Musculoskeletal System - Nordin 4th edition 2012
Category:Foot and Ankle Anatomy
Category:Muscles of the Lower Limb
Musculoskeletal Screening Examination

The GALS (Gait-Arms-Legs-Spine) is a screening examination of the musculoskeletal system. 
==Screening Questions==
* Do you have any pain or stiffness in your arms, legs, or back?
* Do you have any trouble getting up and down stairs or steps?
* Can you dress yourself completely without difficulty?
==Examination==
=== Gait ===
Look for symmetry, smoothness of movement, stride length, pelvic tilt, arm swing, heel strike, stance, toe-off, swing through, and turning. Note specific gait features such as Trendelenburg, antalgic, hemiplegic, Parkinsonian, etc.
=== Arms, Legs and Spine Inspection ===
*From behind 
**Spinal and pelvic alignment
**Paraspinal, shoulder, and gluteal muscle bulk
**Popliteal, foot, or hindfoot swelling.
*From the side
**Spinal curvature
**Schobers test
*From the front
**Shoulder, and quadriceps muscle bulk and symmetry
**Knee swelling
*Mid or hindfoot deformity
=== Arms, Legs, Spine Palpation and Movement ===
*Skin roll over the trapezius
*Cervical spine movement
*Thoracic spine movement
*Lumbar spine movement
*Temporomandibular joint movement
*Sterno-clavicular, gleno-humeral, and acromio-clavicular joint movement
*Elbow extension
=== Wrist and finger deformity or restricted range of motion ===
*Inspection
*Pronation, and supination
*Grip strength
*Fine precision - finger to thumb opposition
*Metacarpal squeeze
=== Supine position ===
*Leg length discrepancy
*Knee movement
*Hip joint movement
*Foot inspection
*Metatarsal squeeze
==External Links==
*https://geekymedics.com/gals-assessment/
Category:Examination
Myofascial Chains

Human anatomy representations typically depict skeletal muscles as separate entities, each with distinct origins and insertions. However, recent studies contest this view, proposing a widespread structural connection between muscles and collagen-rich connective tissues. On a microscopic level, muscle fibers are closely integrated with their endomysium throughout their entire peripheral length. Examining muscles from a macroscopic standpoint reveals a similar pattern, with muscles closely interwoven with surrounding fascia.
The concept of myofascial continuity extends beyond individual muscles and their associated connective tissues. Wilke et al. (2016) conducted a systematic review, analyzing data from 62 cadaver studies, to determine if neighboring muscles are also morphologically linked. The findings suggest strong evidence of continuity in most cases examined. For example, various soft tissues create a continuous pathway from the toes to the occipital bone on the body's dorsal side. This pathway includes fibers of the plantar aponeurosis fusing with the Achilles tendon, which then connects to the gastrocnemius and its fascia. A fascial band connects the calf muscles to the hamstrings at the knee joint, which subsequently attach to the lumbar fascia and the erector spinae muscle via the sacrotuberous ligament. These and other widespread tissue connections, like those on the lateral side, are referred to as "myofascial chains."
A defining characteristic of myofascial chains is the arrangement of components according to muscle fiber direction and lines of pull, contrasting with tissue continuity between parallel muscles (e.g., tibialis anterior and extensor digitorum longus). This arrangement allows for the transfer of greater force. Experimental research on cadavers and in vivo studies support this hypothesis, demonstrating significant interactions between myofascial chain components. Consequently, some researchers believe these chains may be involved in various musculoskeletal disorders.
== Resources ==
Category:Tissues
Myotonia

Myotonia is a feature of some myotonic syndromes such as myotonia congenita and myotonic dystrophy and various other disorders.
== Examination ==
Percussion myotonia is a prolonged muscle contraction lasting several seconds with a sustained dimple appearing on the skin. It is classically tested on the thenar eminence where the thumb may draw into sustained opposition with the fingers.
Normal individuals have percussion irritability where there is a faint transient dimple or ripple at the percussion site. Some normal individuals will also have percussion myoedema where there is a tiny lump at the percussion site.
Muscle contraction myotonia is commonly tested in the hands and eyes. 
For the hands ask the patient to make a tight fist, hold it for 10 seconds, and ask them to open them as quickly as possible. In myotonia the fingers can't open quickly and the wrist flexes involuntarily because of a sustained "after contraction" or delayed relaxation of the wrist flexors.
The the eyes ask the patient to close them as tightly as possible for 5 seconds and then ask to open. The myotonic patient isn't able to open them right away.
== Differential Diagnosis ==
Category:Muscle Disorders
Category:Genetic Disorders
Myotonia Congenita

Myotonia Congenita is a genetic disease characterised by skeletal muscle stiffness from childhood. It sits in a group of disorders known as nondystrophic myotonias to differentiate them from the myotonic dystrophies as the tissues are not dystrophic. It is also known as chloride channel myotonia because it is a chloride channelopathy. The nondystrophic myotonias can be painful and so the Musculoskeletal Physician should be aware of them.
== Genetics ==
There is a loss of function mutation in the CLCN1 gene. Myotonia Congenita can be autosomal dominant which is called Thomsen disease or autosomal recessive which is called Becker disease. The same pathogenic variant can be associated with both forms. 
== Epidemiology ==
The prevalence is 1 in 100,000.
== Clinical Features ==
Patients have episodes of muscle stiffness (myotonia) or cramping that typically begins in childhood. However the age of onset is highly variable. AR myotonia congenita typically occurs later than the AD form, but in both forms the age of onset can be as late as ones 20s to 30s. 
The AR form typically has more severe manifestations including progressive, minor distal weakness, and transient weakness with movement following a period of rest. The stiffness is often alleviated by brief exercise which is called the "warm-up" effect. 
Pain is common but usually not as severe as in myotonic dystrophy type 2. 
Unlike with Myotonic Dystrophy, systemic manifestations do not generally occur. However a minority may have cardiac conduction defects.
On examination there may be percussion myotonia. All skeletal muscle groups can be affected including the eyes, face, and tongue. The muscles may appear hypertrophic.
Clinical Features of AR vs AD Myotonia Congenitahttps://www.ncbi.nlm.nih.gov/books/NBK1355/
Feature 	AR Myotonia Congenita 	AD Myotonia Congenita
Age of onset 	Early childhood 	Early infancy
Muscle stiffness 	Generalized, legs>arms	Generalized, arms>legs
Muscle hypertrophy 	Generalized 	Generalized
Pain 	Very common 	Common
Transient muscle weakness	Common 	Not present
Distal muscle weakness 	Rarely 	Not present
Proximal muscle weakness 	Rarely 	Not present
== Investigations ==
CK is typically elevated <3-4 times the upper limit of normal. EMG may show myotonic bursts.
== Diagnosis ==
The diagnosis is made through molecular genetics by finding a heterozygous pathogenic variant or biallelic pathogenic variants of the CLCN1 gene. There are no clinical diagnostic criteria.
== Differential Diagnosis ==
The following are all the myotonic disorders. The presence of muscle wasting and systemic manifestations suggests myotonic dystrophy.
== Treatment ==
Mexiletine has the best documented effect, which is a sodium channel blocker.
== Resources ==
GeneReviews - Myotonia Congenita
== References ==
Category:Muscle Disorders
Category:Genetic Disorders
Nerves of the Cervical Spine

==Spinal Nerves==
===C1===
The C1 spinal nerve is unique. It does not have a typical dorsal root ganglion. The ganglion cells are located in the rootlets of the spinal accessory nerve. 
The dorsal ramus of C1 is found with the posterior suboccipital muscles. In some individuals there is a cutaneous branch. 
The ventral ramus of C1 runs past the posterior arch of the atlas (C1), behind the superior articular process. It innervates the atlanto-occipital joint and then enters the cervical plexus.
===C2===
The C2 spinal nerve is located behind the lateral atlanto-occipital joint. 
The dorsal ramus supplies the superficial posterior neck muscles, and becomes the greater occipital nerve running over the occiput. 
The ventral ramus innervates the lateral atlantoaxial joint and then joins the cervical plexus.
===C3-C7===
The spinal nerves of C3-C7 are located in their intervertebral foramina. C8 joins them and is found in the C7-T1 foramen.
The ventral rami of C3 and C4 join the cervical plexus. The lower ventral rami join the brachial plexus.
The dorsal rami of the typical spinal nerves form lateral branches that innervate splenius, longissimus, and iliocostalis. The medial branches innervate the cervical zygapophysial joints, and the deeper and medial posterior neck muscles.
==Gray rami communicantes==
Gray rami communicates arise from the stellate ganglion and from the ventral rami of the cervical nerves. They form a plexus which is called the vertebral nerve. The vertebral nerves runs with their vertebral arteries in the transverse foramina and into the posterior cranial fossa.
==Sinuvertebral nerves==
The sinuvertebral nerves of the cervical spine are formed from two roots: the somatic roots from the ventral rami, and teh autonomic roots from the rami communicantes in the vertebral nerve.
The recurrent meningeal branches innervate the dural sac, cervical discs, and posterior longitudinal ligament.
The C1-3 sinuvertebral nerves innervate the ligaments of the median atlantoaxial joint. They then traverse through the foramen magnum and innervate the dura matter overlying the clivus.
Category:Cervical Spine Anatomy
Category:Nerves of the Spine
Neurological Disorders Provoked by Neck Movement

Neurological disorders triggered by head and neck movement represent a diverse spectrum of conditions, ranging from benign and self-limiting to life-threatening pathologies. These disorders involve various mechanisms, such as compression, obstruction, or stretching of critical anatomical structures, and often present with a wide array of symptoms including vertigo, syncope, pain, or abnormal sensations.
== Disorders ==
Disorder 	Characteristics 	Key Symptoms 	Management
Benign Paroxysmal Positional Vertigo (BPPV)	Debris in semicircular canals impeding fluid motion 	Brief vertigo, nystagmus during positional changes 	Epley or Semont maneuvers, avoid vestibular sedatives
Vertebrobasilar Insufficiency 	Posterior circulation ischaemia, possibly due to arterial stenosis 	Vertigo, ataxia, other brainstem or cerebellar symptoms 	Secondary prevention (antiplatelets), avoid provocative movements
Bow Hunter Syndrome 	Extrinsic compression of vertebral artery during neck rotation 	Brainstem/cerebellar symptoms, syncope 	Avoid provocative positions, surgical correction in severe cases
Bruns’ Syndrome 	Mobile intraventricular mass obstructing CSF flow 	Vertigo, headache, nausea/vomiting 	Surgery, antiparasitic medications for neurocysticercosis
Cervical Vertigo 	Controversial; disrupted proprioception from neck 	Dizziness, vertigo 	Diagnosis of exclusion, physiotherapy
Vestibular Paroxysmia 	Compression of vestibular nerve, often by neurovascular conflict 	Short vertigo attacks, triggered by head movement 	Carbamazepine/oxcarbazepine, microvascular decompression if refractory
Carotid Sinus Hypersensitivity 	Excessive vagal response to carotid baroreceptor stimulation 	Syncope, bradycardia 	Pacemaker for cardioinhibitory cases, avoid tight collars
Eagle’s Syndrome 	Compression of carotid artery by elongated styloid process or ossified stylohyoid ligament	Oropharyngeal pain, TIA/stroke from carotid compression 	Conservative management, surgical shortening if severe
Lhermitte’s Phenomenon 	Spinal cord irritation, often in multiple sclerosis 	Electric shock-like sensation radiating down spine 	Treat underlying cause (e.g., MS)
Cervicogenic Headache 	Neck pathology causing headache, e.g. C2/3 zygapophyseal joint pain 	Unilateral headache, worse with neck movement 	Physiotherapy, nerve blocks
Cervical Radiculopathy 	Compression of cervical nerve roots 	Neuropathic pain radiating to the arm 	Analgesia, physiotherapy, decompression surgery for severe cases
Neck-Tongue Syndrome 	Compression of C2 root and hypoglossal nerve 	Neck pain with ipsilateral tongue sensation or posturing	Analgesia, physiotherapy, immobilisation collars
Cervical Arterial Dissection 	Tearing in carotid or vertebral artery walls 	Neck pain, Horner’s syndrome, TIA/stroke 	Antiplatelets/anticoagulants, monitor for TIA/stroke
SSRI Withdrawal ‘Brain Zaps’ 	Abrupt cessation of SSRIs 	Shock-like sensations in head and neck 	Gradual SSRI tapering, restart SSRI if severe
== Resources ==
Category:Neurology
Nondermatomal Somatosensory Deficits

Nondermatomal somatosensory deficits (NDSDs) are sensory deficits that don't conform to the distribution of peripheral nerves or dermatomes, typically seen in the setting of chronic pain and following physical trauma.
== Epidemiology and Risk Factors ==
NDSDs are seen in 25-50% of patients with chronic pain.Mailis-Gagnon A, Nicholson K. On the nature of nondermatomal somatosensory deficits. Clin J Pain. 2011 Jan;27(1):76-84. doi: 10.1097/AJP.0b013e3181e8d9cc. PMID: 20664332. 
A study compared two groups of inpatients with chronic pain, 90 of which had NDSDs and 90 did not. A history of physical trauma was associated with the NDSD group. Personality disorder and adverse childhood experiences was associated with the non-NDSD group. There was no difference in the rates of depression and anxiety.Egloff N, Maecker F, Stauber S, Sabbioni ME, Tunklova L, von Känel R. Nondermatomal somatosensory deficits in chronic pain patients: are they really hysterical? Pain. 2012 Sep;153(9):1847-1851. doi: 10.1016/j.pain.2012.05.006. PMID: 22867972.
== Aetiology ==
The aetiology is usually considered to be functional with a multifactorial aetiology. 
There are certain organic causes for hemisensory syndrome in association with chronic pain such as thalamic stroke. Conditions such as carpal tunnel syndrome commonly present with symptoms and signs that don't conform to known variants of the distribution of the median nerve.
== Clinical Features ==
Sensory Deficits: The onset of the sensory deficit is typically gradual but abrupt presentations can occur. The primary deficits are reduced pinprick sensation, insensitivity to deep tissue pressure, or both. Vicotr Rues. Functional Neurologic Symptom Disorders. Aminoff’s Neurology and General Medicine, Fifth Edition. Elsevier 2014
The distribution may be quadratomal (i.e. one limb) or hemibody on the same side as the chronic pain. In nonorganic causes of hemisensory syndrome there is often an exact splitting at the midline. Certain areas may retain normal sensation within the affected quadratomal or hemibody zone such as the head, nipple, or genitals. The border of the sensory deficit may vary depending on the direction and pattern of the applied stimuli.
Vibration sense may also be impaired. A classic sign of non-organic aetiology in non-organic causes of hemisensory syndrome is loss of vibration sense over one side of the sternum.
Chronic Widespread Pain: The sensory deficits change in association with changes in pain. The pain is often burning or deep aching in quality. The patient is usually more concerned about the pain than the sensory deficit.
Motor Function: There is often an accompanying parallel and unusual alteration in motor function. However anaesthetic hands often retain the ability for complex delicate movements.
== Diagnosis ==
The clinician should have some caution in applying the term "nondermatomal," firstly because of the myriad of anatomical variations, and secondly because such sensory deficits may resolve upon effective treatment of the primary pain condition.
== References ==
Category:Neurology