Specific populations at high risk of primary PFPS include runners, bicyclists, basketball players, young athletes and females.

Trendelenburg's sign is found in people with weak or paralyzed abductor muscles of the hip, namely gluteus medius and gluteus minimus. It is named after the German surgeon Friedrich Trendelenburg.

The gluteus medius is very important during the stance phase of the gait cycle to maintain both hips at the same level. Moreover, one leg stance accounts for about 60% of the gait cycle. Furthermore, during the stance phase of the gait cycle, there is approximately three times the body weight transmitted to the hip joint. The hip abductors' action accounts for two thirds of that body weight. The Trendelenburg sign is said to be positive if, when standing on one leg, the pelvis drops on the side opposite to the stance leg to reduce the load by decreasing the lever arm. By reducing the lever arm, this decreases the work load on the hip abductors. The muscle weakness is present on the side of the stance leg. A Trendelenburg sign can occur when there is presence of a muscular dysfunction (weakness of the gluteus medius or minimus) or when someone is experiencing pain. The body is not able to maintain the center of gravity on the side of the stance leg. Normally, the body shifts the weight to the stance leg, allowing the shift of the center of gravity and consequently stabilizing or balancing the body. However, in this scenario, when the patient/person lifts the opposing leg, the shift is not created and the patient/person cannot maintain balance leading to instability.

In most patients with PFPS an examination of their history will highlight a precipitating event that caused the injury. Changes in activity patterns such as excessive increases in running mileage, repetitions such as running up steps and the addition of strength exercises that affect the patellofemoral joint are commonly associated with symptom onset. Excessively worn or poorly fitted footwear may be a contributing factor. To prevent recurrence the causal behaviour should be identified and managed correctly.

The medical cause of PFPS is thought to be increased pressure on the patellofemoral joint. There are several theorized mechanisms relating to how this increased pressure occurs:

- Increased levels of physical activity

- Malalignment of the patella as it moves through the femoral groove

- Quadriceps muscle imbalance

- Tight anatomical structures, e.g. retinaculum or iliotibial band.

The cause of pain and dysfunction often results from either abnormal forces (e.g. increased pull of the lateral quadriceps retinaculum with acute or chronic lateral PF subluxation/dislocation) or prolonged repetitive compressive or shearing forces (running or jumping) on the PF joint. The result is synovial irritation and inflammation and subchondral bony changes in the distal femur or patella known as "bone bruises". Secondary causes of PF Syndrome are fractures, internal knee derangement, osteoarthritis of the knee and bony tumors in or around the knee.

Most commonly due to anterior shoulder dislocation caused by hyperabduction and external rotation of the arm. Usually in young men who play contact sports (E.g. rugby, football, volleyball, basketball, etc.). Frequent anterior (frontward) subluxation also poses a great risk factor.

Humeral avulsion of the glenohumeral ligament (HAGL) is defined as an avulsion (tearing away) of the inferior glenohumeral ligament from the anatomic neck of the humerus. In other words, it occurs when we have disruption of the ligaments that join the humerus to the glenoid.

HAGL tends to occur in 7.5-9.3% of cases of anterior shoulder instability. Making it an uncommon cause of anterior shoulder instability.

Avulsion of this ligamentous complex may occur in three sites: glenoid insertion (40%), the midsubstance (35%) and the humeral insertion (25%).

Gluteal gait is an abnormal gait caused by neurological problems. If the superior gluteal nerve or obturator nerves are injured, they fail to control the gluteus minimus and medius muscles properly, thus producing an inability to tilt the pelvis upward while swinging the leg forward to walk. To compensate for this loss, the leg swings out laterally so that the foot can move forward, producing a shuffling or waddling gait.

Injury to the superior gluteal nerve results in a characteristic motor loss, resulting in a disabling gluteus medius limp, to compensate for weakened abduction of the thigh by the gluteus medius and minimus, and/or a gluteal gait, a compensatory list of the body to the weakened gluteal side.

As a result of this compensation, the center of gravity is placed over the supporting lower limb. Medial rotation of the thigh is also severely impaired. When a person is asked to stand on one leg, the gluteus medius and minimus normally contract as soon as the contralateral foot leaves the floor, preventing tipping of the pelvis to the unsupported side. When a person with paralysis of the superior gluteal nerve is asked to stand on one leg, the pelvis descends on the unsupported side, indicating that the gluteus medius on the contralateral side is weak or non-functional. This observation is referred to clinically as a positive Trendelenburg's sign.

When the pelvis descends on the unsupported side, the lower limb becomes, in effect, too long and does not clear the ground when the foot is brought forward in the swing phase of walking. To compensate, the individual leans away from the unsupported side, raising the pelvis to allow adequate room for the foot to clear the ground as it swings forward.

Joint stiffness may be either the symptom of pain on moving a joint, the symptom of loss of range of motion or the physical sign of reduced range of motion.

- Pain on movement is commonly caused by osteoarthritis, often in quite minor degrees, and other forms of arthritis. It may also be caused by injury or overuse and rarely by more complex causes of pain such as infection or neoplasm. The range of motion may be normal or limited by pain. "Morning stiffness" pain which eases up after the joint has been used, is characteristic of rheumatoid arthritis.

- Loss of motion (symptom): the patient notices that the joint (or many joints) do not move as far as they used to or need to. Loss of motion is a feature of more advanced stages of arthritis including osteoarthritis, rheumatoid arthritis and ankylosing spondylitis.

- Loss of range of motion (sign): the examining medical professional notes that the range of motion of the joint is less than normal. Routine examination by an orthopaedic surgeon or rheumatologist will often pay particular attention to this. The range of motion may be measured and compared to the other side and to normal ranges. This sign is associated with the same causes as the symptom. In extreme cases when the joint does not move at all it is said to be ankylosed.

Trousseau sign of latent tetany is a medical sign observed in patients with low calcium. From 1 to 4 percent of normal patients will test positive for Trousseau's sign of latent tetany. This sign may be positive before other manifestations of hypocalcemia such as hyperreflexia and tetany, as such it is generally believed to be more sensitive (94%) than the Chvostek sign (29%) for hypocalcemia.

To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct. The sign is also known as main d'accoucheur (French for ""hand of the obstetrician"") because it supposedly resembles the position of an obstetrician's hand in delivering a baby.

The sign is named after French physician Armand Trousseau who described the phenomenon in 1861. It is distinct from the Trousseau sign of malignancy.

Tinel's sign is a way to detect irritated nerves. It is performed by lightly tapping (percussing) over the nerve to elicit a sensation of tingling or "pins and needles" in the distribution of the nerve. It takes its name from French neurologist Jules Tinel (1879–1952).

For example, in carpal tunnel syndrome where the median nerve is compressed at the wrist, Tinel's sign is often "positive" causing tingling in the thumb, index, middle finger and the radial half of the fourth digit. Tinel's sign is sometimes referred to as "distal tingling on percussion" or DTP. This distal sign of regeneration can be expected during different stage of somatosensory recovery.

Although most frequently associated with carpal tunnel syndrome, Tinel's sign is a generalized term, and can also be positive in tarsal tunnel syndrome, or in ulnar nerve impingement at the wrist (Guyon's canal syndrome), where it affects the other (ulnar) half of the fourth digit and the fifth digit.

Tetany or tetany seizure is a medical sign consisting of the involuntary contraction of muscles, which may be caused by disease or other conditions that increase the action potential frequency of muscle cells or the nerves that innervate them. Muscle cramps which are caused by the disease tetanus are not classified as tetany; rather, they are due to a lack of inhibition to the neurons that supply muscles.

French Professor Armand Trousseau (1801-1867) devised the trick (now known as the Trousseau sign of latent tetany) of occluding the brachial artery by squeezing, to trigger cramps in the fingers. Also, tetany can be demonstrated by tapping anterior to the ear, at the emergence of the facial nerve. A resultant twitch of the nose or lips suggests low calcium levels. This is now known as the Chvostek sign.

Tetany is characterized by contraction of distal muscles of the hands (carpal spasm with extension of interphalangeal joints and adduction and flexion of the metacarpophalangeal joints) and feet (pedal spasm) and is associated with tingling around the mouth and distally in the limbs.

EMG studies reveal single or often grouped motor unit discharges at low discharge frequency during tetany episodes.

The occurrence (incidence) on abdominal or chest X-rays is around 0.1% but it can be up to 1% in series of older adults. It has also been reported in children.

The exact cause is not always known, but it may occur in patients with a long and mobile colon (dolichocolon), chronic lung disease such as emphysema, or liver problems such as cirrhosis and ascites. Chilaiditi's sign is generally not associated with symptoms, and is most commonly an incidental finding in normal individuals.

Absence or laxity of the ligament suspending the transverse colon or of the falciform ligament are also thought to contribute to the condition. It can also be associated with relative atrophy of the medial segment of the left lobe of the liver. In this case, the gallbladder position is often anomalous as well – it is often located anterior to the liver, rather than posterior.

An upper motor neuron lesion (also known as pyramidal insufficiency) occurs in the neural pathway above the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves. Conversely, a lower motor neuron lesion affects nerve fibers traveling from the anterior horn of the spinal cord or the cranial motor nuclei to the relevant muscle(s).

Upper motor neuron lesions occur in the brain or the spinal cord as the result of stroke, multiple sclerosis, traumatic brain injury and cerebral palsy.

The Chvostek sign () is a clinical sign of existing nerve hyperexcitability (tetany) seen in hypocalcemia. It refers to an abnormal reaction to the stimulation of the facial nerve. When the facial nerve is tapped in front of tragus the facial muscles on the same side of the face will contract momentarily (typically a twitch of the nose or lips) because of hypocalcemia (i.e. from hypoparathyroidism, pseudohypoparathyroidism, hypovitaminosis D) with resultant hyperexcitability of nerves. Though classically described in hypocalcemia, this sign may also be encountered in respiratory alkalosis, such as that seen in hyperventilation, which causes decreased serum Ca with a normal calcium level due to a shift of Ca from the blood to albumin which has become more negative in the alkalotic state.

The Trousseau sign of latent tetany is also often used to detect early tetany.

Chvostek's sign is found in tetany.

It may also be present in hypomagnesemia, Magnesium is a cofactor for Adenylate cyclase. The reaction that Adenylate cyclase catalyzes is the conversion of ATP to 3',5'-cyclic AMP. The 3',5'-cyclic AMP (cAMP) is required for parathyroid hormone activation. It is frequently seen in alcoholics, persons with diarrhea, patients taking aminoglycosides or diuretics, because hypomagnesemia can cause hypocalcemia. It is also seen in measles, tetanus and myxedema.

It can also be found in subjects with respiratory alkalosis, for example as a result of hyperventilation syndrome, which can lead to a drastic reduction of the concentration in serum of calcium ions while at normal levels, for the binding of a significant proportion of ionized calcium (Ca 2+ ) with albumin and globulins.

Raccoon eye/eyes (also known in the United Kingdom and Ireland as panda eyes) or periorbital ecchymosis is a sign of basal skull fracture or subgaleal hematoma, a craniotomy that ruptured the meninges, or (rarely) certain cancers. Bilateral hemorrhage occurs when damage at the time of a facial fracture tears the meninges and causes the venous sinuses to bleed into the arachnoid villi and the cranial sinuses. In layman's terms, blood from skull fracture seeps into the soft tissue around the eyes. Raccoon eyes may be accompanied by Battle's sign, an ecchymosis behind the ear. These signs may be the only sign of a skull fracture, as it may not show on an X-ray. They may not appear until up 2–3 days after the injury. It is recommended that the patient not blow their nose, cough vigorously, or strain to prevent further tearing of the meninges.

Raccoon eyes may be bilateral or unilateral. If bilateral, it is highly suggestive of basilar skull fracture, with a positive predictive value of 85%. They are most often associated with fractures of the anterior cranial fossa.

Raccoon eyes may also be a sign of disseminated neuroblastoma or of amyloidosis (multiple myeloma).

Depending on cause, raccoon eyes always require urgent consultation and management, that is surgical (facial fracture or post-craniotomy) or medical (neuroblastoma or amyloidosis).

Hutchinson's pupil is a clinical sign in which the pupil on the side of an intracranial mass lesion is dilated and unreactive to light, due to compression of the oculomotor nerve on that side. The sign is named after Sir Jonathan Hutchinson.

These can be due to concussion injury to the brain and is associated with subdural haemorrhage and unconsciousness.

The parasympathetic fibers to the pupil are responsible for pupillary constriction. The fibers pass through the periphery of the oculomotor nerve, and hence are the first to be affected in case of compression of the nerve. In Stage 1, the parasympathetic fibers on the side of injury are irritated, leading to constriction of pupil on that side. In stage 2, the parasympathetic fibers on the side of injury are paralysed, leading to dilatation of pupil. The fibers on the opposite oculomotor nerve are irritated, leading to constriction on opposite side. In stage 3, the parasympathetic fibers on both sides are paralysed - leading to bilateral pupillary dilatation. Pupils become fixed. This could typically indicates a very serious underlying condition.

A chignon is a temporary swelling left on an infant's head after a ventouse suction cap has been used to deliver him or her. It is not a sign of serious injury and may take as little as two hours or as long as two weeks to disappear.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.

Changes in muscle performance can be broadly described as the upper motor neuron syndrome. These changes vary depending on the site and the extent of the lesion, and may include:

- Muscle weakness. A pattern of weakness in the extensors (upper limbs) or flexors (lower limbs), is known as 'pyramidal weakness'

- Decreased control of active movement, particularly slowness

- Spasticity, a velocity-dependent change in muscle tone

- Clasp-knife response where initial higher resistance to movement is followed by a lesser resistance

- Babinski sign is present, where the big toe is raised (extended) rather than curled downwards (flexed) upon appropriate stimulation of the sole of the foot. The presence of the Babinski sign is an abnormal response in adulthood. Normally, during the plantar reflex, it causes plantar flexion and the adduction of the toes. In Babinski's sign, there is dorsiflexion of the big toe and abduction of the other toes. Physiologically, it is normally present in infants from birth to 12 months. The presence of the Babinski sign after 12 months is the sign of a non-specific upper motor neuron lesion.

- Increased deep tendon reflex (DTR)

- Pronator drift

Hutchinson's mask is a patient's sensation that the face is covered with a mask or a gauzy network like cobwebs. This medical sign is associated with tabes dorsalis affecting the trigeminal nerve (fifth cranial nerve CN V). It is named in honour of the English physician Sir Jonathan Hutchinson (1828–1913).

Causes include

- Acute pancreatitis, whereby methemalbumin formed from digested blood tracks subcutaneously around the abdomen from the inflamed pancreas.

- Pancreatic hemorrhage

- Retroperitoneal hemorrhage

- Blunt abdominal trauma

- Ruptured / hemorrhagic ectopic pregnancy.

- Spontaneous bleeding secondary to coagulopathy (congenital or acquired)

- Aortic rupture, from ruptured abdominal aortic aneurysm or other causes.

Thrombophlebitis occurs almost equally between women and men, though males do have a slightly higher possibility. The average age of developing thrombophlebitis, based on analyzed incidents, is 54 for men and 58 for women.