Superficial Abdominal reflexes -A complete guide

Definition
An abdominal reflex is a superficial neurological reflex that is elicited by  by stroking the abdomen around the umbilicus. It is a reflex with localising value in neurology.As it is a superficial reflex, it is polysynaptic.
Prerequisites for elicitation of abdominal reflex

• Palpate the abdomen lor the degree of relaxation 
• Explain the procedure to the patient
• Apply  light non painful stimulus along the line of contraction of the muscle  
• Stimulus should not be unpleasant

Method  of elicitation
The patient should lie flat, palpate the abdomen gently to assess the degree of relaxation and sensitivity of the skin. Then explain the procedure and illustrate on the chest.Lightly stroke the abdomen with a blunt object either a key or two point discriminator from without inwards, stimulating each of the four quadrants of the abdomen.
Normal response:There is homolateral contraction of the abdominal muscles and retraction of the linea alba and the umbilicus towards the area stimulated.



Root value of abdominal reflex
Superficial abdominal reflex center- T7 to T 12 spinal segments
Afferent is  posterior  root and efferent  is anterior  root of spinal nerves T7 to T12

• Upper abdominal -T6-T8
• Mid abdominal—T8-T10
• Lower abdominal - T10-T12

What  are the types of Abdominal Reflex
1.Normal abdominal reflex
2.Absent abdominals
3.Fatiguable abdominals
4.Exaggerated abdominals
Exaggerated abdominal reflexes may be seen in psycho neurosis, or in anxiety states
5.Dissociated abdominals
In UMN lesion the superficial abdominal reflex is absent while the deep abdominal reflex is exaggerated.


6.Inverted abdominals
It is seen in unilateral abdominal paralysis
Stimulation of the paralysed side leads to contraction of the normal side & deviation of umbilicus to that side while the reflex is absent on the paralysed side
When Beevor's sign is positive, there is upper abdominal muscle contraction and retained upper abdominal reflexes.but there is absence of lower abdominal muscle contraction and reflexes (T10 - segment lesion).
Fallacies

• Heavy stimulation will elicit a deep abdominal reflex which is often exaggerated in a corticospinal tract lesion
• Lax or tense abdomen may result in absent abdominals
• Abdominals are not always absent in multiple sclerosis
• Difficulty in relaxing the abdominals may be circumvented by eliciting the jerk while the patient is upright
• If the abdomen is lax, slight contraction can still be elicited by stimulation near the ribs and-inguinal ligament
• Abdominal reflexes are retained till late in a motor neurondisease, cerebral diplegia, infantile hemiplegia inspite ot pyramidal system involvement.
• There is unilateral loss of abdominal reflexes on the side of hemiplegia.

What are the causes of absent Abdominal reflex ?

Absent abdominal reflex is observed in the following condition
Corticospinal tract lesion but it may not be absent in all case
Fatiguable Abdominal
Subtle corticospinal tract lesion
Defects of technique, relaxation, or observation- Tense abdomen
A break in the appropriate reflex arc

• Motor root
• Sensory root
• Peripheral nerve-It can occur due to lesions such as herpes-zoster, or scar due to surgical operations  that have damaged the peripheral nerves or the muscle itself.

Lax abdomen-Repeated pregnancies (multigravid woman), in patients with flaccid abdominal muscles,
Distention of abdomen (ascites, pregnancy or massive organomegaly)
Pyramidal system lesions above the upper level of segmental innervation.

Superior orbital fissure syndrome:clinical features and causes

The term superior orbital fissure syndrome (SOFS) also called as Rochon–Duvigneaud syndrome is applied to lesions located immediately anterior to the orbital apex, including the structures exiting the annulus of Zinn and often those external to the annulus.

This syndrome is characterised by Multiple cranial nerve palsies may be seen i

• Oculomotor nerve (III)
• Trochlear nerve (IV)
• Abducens nerve (VI) 
• Ophthalmic branch of the trigeminal nerve (V1)
• In the absence of optic nerve pathology

The syndrome is characterised by  retro-orbital paralysis of extraocular muscles  impairment of the branches of the 1st division of the trigeminal nerve and frequently extension to involve the optic nerve.

Examination shows ophthalmoplegia, ptosis, decreased corneal sensation, and occasionally visual loss caused by mechanical optic nerve compression. The presence of proptosis, with swelling of eyelids and chemosis (swelling of ocular surface membranes), indicates significant mass extension within the orbit.

The clinical features  are 

• Pupillary dilation via alteration in cranial nerve III function in it's innervation of the pupillary constrictors.
• Ptosis - Cranial nerve III involvement causes paresis of the levator palpebrae superiorus muscle
• Pain
• Proptosis from engorgement of the ophthalmic vein and lymphatics.
• Extraocular Paresis of cranial nerves III, IV, and VI causing ophthalmoplegia.
• Parasthesia  injury to the first division of cranial nerve V with hypesthesia of the supraorbital and supratrochlear nerves 
• Loss of the corneal Reflex.

The orbital apex syndrome is characterised by all of the above plus optic nerve involvement, leading to changes in visual acuity

Potential causes  of superior orbital fissure syndrome include

• Traumatic craniomaxillofacial injuries
• Tumours of the orbit (lymphoma or rhabdomyosarcoma) and adjacent structures
• Infection- Fungal infection of the orbit is an important though rare cause of an orbital apex syndrome and is usually secondary to sinus involvement.
• Inflammatory disorders, and vasculitic   ischaemic diseases. Orbital inflammation may be isolated (non-specific orbital inflammation), or associated with systemic inflammation such as Wegener’s granulomatosis, polyarteritis nodosa, sarcoidosis, or, rarely, temporal arteritis.

Laboratory workup could include:

• Complete blood count (CBC)
• Erythrocyte sedimentation rate (ESR)
• C reactive protein
• Electrolytes
• Blood glucose
• Antinuclear antibody (ANA)
• Extractable nuclear antibodies (ENA)
• Antineutrophilic antibody -ANCA
• Serum protein electrophoresis
• Borrelia serology,
• Serum angiotensin converting enzyme (ACE).
• Cerebrospinal fluid (CSF) examination (infections, granulomatous disease, and malignancy) can be helpful.
• Biopsy may be necessary but is technically challenging and only considered after a trial of treatment with steroids with no initial response or following early relapse.

What are the causes of Babinski sign in absence of Pyramidal Tract Lesion

Babinski sign in absence of Pyramidal Tract Lesion can occur in physiological and pathological conditions

Physiological causes of Babinski sign in absence of Pyramidal Tract Lesion

• Infancy (up to 1 year of age)
• Deep sleep
• Deep anaesthesia

Pathological causes of Babinski sign in absence of Pyramidal Tract Lesion

• Narcotic overdose
• Alcohol intoxication
• Following electroconvulsive therapy
• Coma secondary to metabolic disturbances
• Post-traumatic states
• Post-ictal state
• In Cheyne-Stokes respiration, the extensor response may appear during the period of apnoea, whereas in the phase of active respiration the normal reflex is seen.

What is the normal plantar response ?

The normal response is 'flexor in type and is manifested by the following components :

• Flexion of all the flve toes.
• Dorsiflexion and inversion of the foot.
• Flexion of the knee and the hip.
• Contraction of adductors of the thigh, sartorius and tensor fascia lata (minimal response)

Cremasteric reflex- clinical significance

Cremasteric reflex  is a  polysynaptic reflex, the afferent fibers extend to cortex, descending fibers to anterior horn cells are through or close to pyramidal tract. Hence in pyramidal lesion, the reflex arc is disrupted. ,
Pre requisites for eliciting cremasteric reflex

• Expose the testes
• Stimulus is given from  above downwards

Method  of elicitation
Upper inner part of the thigh is stroked in a downward and inward direction with a blunt point, in the supine position, watch the movement of testicle and scrotum.
Response of reflex
Contraction of the this muscle pulls up the scrotum and testicle on the side examined cremasteric  muscle.The contraction of the cremasteric muscle pulls up the scrotum and the testicle upwards on the side examined
Reflex arc of cremasteric reflex

• Afferent:Femoral nerve(Ilioinguinal nerve)
• Segment -L2
• Efferent:Genitofemoral

Root Value
• LI-L2
Abnormal response

• Absence of cremasteric reflex – seen in elderly, pyramidal lesion, any break in the reflex arc
• Local diseases like hydrocoele, epididymoorchitis

Fallacies
Cremasteric reflex should be differentiated from a scrotal reflex which is due to the contraction of the dartos muscle.

Superior orbital fissure and its contents

The superior orbital fissure is the communication between the cavernous sinus and the apex of the orbit. It is straddled by the tendinous ring which is the common origin of the four rectus muscles .The superior orbital fissure is a foramen in the skull, although strictly it is more of a cleft, situated between the lesser and greater wings of the sphenoid bone.
Boundaries of superior orbital fissure
Medial border is formed by body of sphenoid
Superior border is formed by: lesser wing of sphenoid
Inferior border formed by : greater wing of sphenoid.
Lateral border is formed by : frontal bone
What are the structures passing through superior orbital fissure?
A number of important anatomical structures pass through the fissure. These structures are:

• Superior and inferior divisions of oculomotor nerve (III)
• Trochlear nerve (IV)
• Lacrimal, frontal and nasociliary branches of ophthalmic (V1).
• Abducent nerve (VI)
• Superior and inferior divisions of ophthalmic vein. Inferior division also passes through the  inferior orbital fissure.
• Sympathetic fibers from cavernous plexus

SOF is divided into 3 parts from lateral to medial.
For practical purpose SOF is divided into lateral ,middle and medial part.each transmit its own contents
Lateral part of superior orbital fissure transmits the following :

• Superior ophthalmic vein, 
• Lacrimal nerve, frontal nerve (branch of the ophthalmic division of the trigeminal nerve)
• Trochlear nerve (CN IV), 
• Recurrent meningeal branch of lacrimal artery (anastomotic branch of lacrimal artery with the  middle meningeal artery)

Middle part  of SOF transmits the following

• Superior and inferior divisions of the oculomotor nerve (CN III), 
• Nasociliary nerve (a branch of the ophthalmic division of the trigeminal nerve) lies between the two divisions of oculomotor nerve 
• Abducent nerve

Medial part of SFO  transmits the following

• Inferior ophthalmic veins
• Sympathetic nerves arising from the plexus that accompanies the internal carotid artery

Contents - Through the fissure (from superior to inferior) pass:

• Lacrimal nerve (a branch of the ophthalmic division of the trigeminal nerve).
• Frontal nerve (a branch of the ophthalmic division of the trigeminal nerve).
• Superior ophthalmic vein.
• Trochlear nerve (CN IV).
• Superior division of the oculomotor nerve (CN III).
• Nasociliary nerve (a branch of the ophthalmic division of the trigeminal nerve)
• Inferior division of the oculomotor nerve (CN III)
• Abducens nerve (CN VI)
• A branch of the inferior ophthalmic vein

Bulbocavernosus reflex -Clinical significance

It is a superficial reflex that is useful  in paraplegia.The bulbocavernosus reflex is an oligosynaptic reflex mediated through the S2–S4 spinal cord segments

Method of elicitation 

This reflex can be elicited by pinching on the glans penis or pulling on the catheter with one hand the other hand is placed over the perineum at the root of the penis

Normal Response

Normal response is the reflex contraction of the bulbospongiosus muscle the muscle is felt at the junction of the penis and the scrotum.

Abnormalities  of  bulbocavernous reflex

Bulbocavernous reflex is absent in

• Lesion of the local reflex arch of S2-S4
• Pyramidal lesions

Clinical significance

1.It is a superficial reflex which  has localising value in paraplegia

2.The bulbocavernosus reflex is one of the few ways to test the following

       Conus medullaris (which is the distal end of the spinal cord)

       The S2 to S4 pelvic nerves (the only other bedside test of this region is testing sensation in the             perineal, or “saddle,” area).

3.This reflex is particularly important in patients with urinary retention, that is caused by disease of the pelvic nerves or cauda equina.

This reflex is useful to differentiate between UMN and LMN bladder.

• UMN bladder—reflex preserved
• LMN bladder reflex lost

The advantage of bulbocavernosus reflex monitoring is that it will tests the functional integrity of the three different anatomic structures:

In spinal cord injury above the S2 to S4 level (i.e., lesion of upper motor neurons innervating the S2 to S4 segment), the bulbocavernosus reflex also disappears, but only temporarily for a period of 1 to 6 weeks.

Prognostic significance

• Complete absence of distal motor or sensory function or perirectal sensation, together with recovery of the bulbocavernosus reflex  indicates a complete cord injury, and in such cases it is highly unlikely that significant neurologic function will ever return.
• Therefore, if no motor or sensory recovery below the level of  lesion is present, patient has a complete spinal cord injury and no further distal recovery of motor function can be expected;
• On other hand, any spared motor or sensory function below level of injury is considered incomplete spinal cord injury , potential for recovery of incomplete lesion is determined by part of the cord most severely injured
• Following spinal cord trauma, presence or absence of this reflex carries prognostic significance;
• In cases of cervical or thoracic cord injury, absence of this reflex documents continuation of spinal shock or spinal injury at the level of  the reflex arc itself;
• Period of spinal shock usually resolves  within a period of  48 hours and return of bulbocavernosus reflex is a good signals fo termination of spinal shock;
• Remember that spinal shock does not apply to lesions that occur below the cord, and therefore, low lumbar burst fracturers should not cause spinal shock (and in this situation, the absence of the bulbocaveronsus reflex indicates that there is a cauda equina injury)
• Persistent loss of the bulbocavernosus reflex may be a result of a conus medullaris injury (eg from an L1 burst fracture )

Root Value of bulbocavernous 

Bulbocavernous reflex is innervated by  S3.S4

The afferent paths of the bulbocavernosus reflex are the sensory fibers of the pudendal nerves

The reflex center in the S2–S4 spinal segment. 

The efferent paths are the motor fibers of the pudendal nerves and anal sphincter muscles

What is Equivocal Babinski Sign?

Plantar response is a very important clinical sign in neurology which indicate pyramidal tract lesion
Equivocal babiski sign is an incomplete response.Occur when all the omponents of extensor plantar response is not manifested.
Plantar response is said to be equivocal in following situations:

• There is a rapid but brief extension of toes at first,which is followed by flexion or predominant flexion' followed by extension.
• There is only extension of great toe or extension of great toe with flexion of other toes
• There is no response to plantar stimulation, particularly if there is paralysis of dorsiflexors.
• There may be flexion of knee and hip with no movement of toes.
• There is only fanning out of toes and there is no movement of big toe
• Absent plantar response on the hemiplegic sign and flexor response on the normal side.This may be an early sign of Cerebrovascular accident

Todays equivocal response may be tomorrows extensor response.

Types of Babinski sign

Introduction
The plantar reflex (PR) is one of the most useful  reflex in the body;. It is basically a polysynaptic superficial reflex, designed to withdraw the stimulated part, i.e., the foot from a potentially dangerous stimulus. Joseph Babinski, a French neurologist, first differentiated between a normal and a pathologic plantar response and described the Babinski sign in 1896
The Babinski’s sign 
It is seen  in patients with pyramidal tract dysfunction and is characterised by a dorsiflexion or extension of the great toe with or without fanning or abduction of the other toes. The fully developed response is characterised  by

• Dorsiflexion of the ankle 
• Flexion of the hip   Knee joint 
• Slight abduction of the thigh, leading to a withdrawal of the leg on plantar stimulation.

x
1.True Babinski sign 
 It includes all the components of the fully developed extensor plantar response.link
2.Minimal Babinski sign 
 It is characterised by contraction of the hamstring muscles and the tensor fasciae latae which can   be detected by palpation of the thigh.
 3.Exaggerated Babinski sign :
 It can either be in the form of 'flexor spasm' or 'extensor spasm', depending upon the muscles i.e. whether flexors or extensors, have excess of tone.
 Flexor spasms can occur in the following conditions

•  Spinal cord disease
•  Bilateral upper motor neuron lesion at a supraspinal level
•  Multiple sclerosis
•  Subacute combined degeneration of the cord

Flexor spasms can occur in patients with bilateral UMN lesion at the supraspinal or spinal cord level. Extensor spasms can occur in patients with bilateral corticospinal tract lesion but preserved posterior column function.
4.Spontaneous Babinski sign 
This is seen in infants and children following manipulation of the foot. It is seen in patients with extensive pyramidal tract lesions. Passive flexion of the hip and knee or passive extension of the knee may produce a positive Babinski sign in adults
5. Pseudo Babinski sign 
6.Crossed extensor response/bilateral Babinski sign
This is seen in cases with bilateral cerebral lesions
Unilateral stimulation will  bilateral  Babinski in patients with bilateral cerebral disease and spinal cord disease.r spinal cord disease.
7.Tonic Babinski reflex
It is characterised by a slow prolonged contraction of the toe extensors. observed with combined frontal lobe lesions and extrapyramidal involvement.
This is  seen in frontal lobe lesions and extrapyramidal involvement.
8. Inversion of plantar reflex :
If the short flexors of the toe are paralysed or flexor tendons are severed accidentally, an extensor response may be observed

What is Pseudo-Babinski Sign?

The plantar reflex (PR) is one of the most important reflex in the body. It is basically a polysynaptic superficial reflex, designed to withdraw the stimulated part, i.e., the foot from a potentially dangerous stimulus
Joseph Babinski, a French neurologist, first differentiated between a normal and a pathologic plantar response and he described the Babinski sign in 1896. The Babinski’s sign is observed in patients with pyramidal tract dysfunction and is characterised by a dorsiflexion or extension ofthe the ankle and flexion of the hip and knee joint and slight abduction of the thigh,
leading to a withdrawal of the leg on plantar stimulation

False Babinski sign may sometimes occur in the absence of pyramidal tract lesion. This may be seen in the following conditions.

• A voluntary withdrawal in overtly sensitive individuals on attempting to stroke the sole of the foot.
• As a response in plantar hyperesthesia
• Application of a strong or painful stimulus to the sole of the foot.
• In the presence  of chorea, where the big toe may extend as a response to dystonic posturing.
• If the short flexors of the toes are paralyzed (due to lower motor neuron lesion), there may be an inversion of the plantar reflex.

Differentiation between Babinski and Pseudo-Babinski Sign

• Contraction of hamstring muscles can be felt in Babinski sign. There is no associated contraction of the hamstring muscles in pseudo babinski
• Pressure on the base of the great toe while eliciting the plantar reflex does not inhibit the extensor in Babinski sign.Pressure on the base of the great toe while eliciting the plantar response will inhibit the withdrawal extensor response

What is Pseudoclonus?

Clonus (from the Greek for "violent, confused motion") is a series of involuntary, rhythmic, muscular contractions and relaxations. Clonus is a sign of certain neurological conditions, particularly associated with upper motor neuron lesions affecting the descending motor pathways, and in most cases is, accompanied by spasticity (another form of hyperexcitability).
The clonus is  sustained inspite of a steady pressure,this is seen in pseudoclonus
It is irregular in rate (usually less than 6 at a time) and rhythm.
It is commonly seen in anxiety, in tense persons, often in hysteria and thyrotoxicosis.
Plantar response is always flexor.
Many a time, the boundary between true and pseudoclonus is not very clear.

Patellar clonus - clinical significance

Patellar clonus is a clinical sign of pyramidal tract dysfunction.It is usually associated with exaggerrated reflex and extensor plantar reflex.
How to elicit the patellar clonus?

• Patient lies supine with knee extended.
• Fix the leg with one hand
• Patella is pulled upwards with a fold of  skin behind the palm.
• Now a sharp and sudden displacement of the patella downwards by the index finger and thumb( sustained pressure is applied) will produce series of quadriceps contraction.

It is also known as knee clonus.

Significance

It is seen in pyramidal tract lesions

Ankle and patellar clonus are produced as a result of loss of upper motor control (ie. UMN lesion) over S1 

Babinski's Sign or Extensor Plantar Response

The Babinski sign can indicate upper motor neuron lesion constituting damage to the corticospinal tract

In 1896 Babinski first described this sign.

Joseph Francois Felix Babinski was a French physician cum neurologist. It is considered as the sign in Neurology

The response are dorsiflexion and extension of great toe.The movement occur at the metatarsophalangeal joint.This is the first movement that precedes all the other movements 

On eliciting the plantar response, there is dorsiflexion of the great toe, along with extension and fanning out of the other toes.

In addition, especially if the extensor response is marked, there is dorsiflexion at the ankle, with flexion at the knee and hip, these associated movements being brought about by contraction of the anterior tibial. hamstrings, and tensor fascia lata.

The Babinski's sign can be elicited only by stroking the lateral aspect of the dorsum of foot in the following situations.

• Presence of minimal pyramidal tract lesion, 
• In individuals with thick soles.

The Babinski sign can be elicited over the medial aspect of the foot when the lesion becomes dense (this is due to increase in the reflexogenic area).

If no plantar response can be elicited with the patient's knee flexed and thigh externally rotated, it can be elicited by extending the patient's knee, or even applying pressure on the knee (thigh being in the neutral position). .

With repeated stimulation of the sole of the foot, the plantar response may become fatigued, and the extensor plantar response may not be elicitable.

The components of extensor plantar response is 

Components are 

• Extension of big toe
• Extension of other toes and fanning
• Dorsiflexion and eversion
• Flexion of knee and hip joint. 

The only visible response may be dorsiflexion of big toe, contraction of other muscles can be felt by palpation.

Finger flexion response

It is an deep tendon reflex of upperlimb .It is exaggerated in pyramidal ract lesion
Method of elicitation of finger flexion response

• Allow the patient's hand to rest with palm upwards, the fingers slightly flexed
• The tips of your middle and index lingers are placed across the palmar surfaces of the proximal phalanges of the patient s fingers
• The examiner gently interlocks his fingers with the patient's and strikes them with knee hammer
• A sudden tap on your fingers with the hammer on the palmar aspect of fingers  produces slight flexion of all fingers, but a very brisk contraction indicates hyperreflexia.

Innervation of finger flexion response
The root value of this reflex is C7 C8 T1

Nerve involved  - median and ulnar nerve

Clinical significance of fingerflexion response
There is no precise hand equivalent for the plantar response, however, the finger flexor reflexes can help demonstrate hyperreflexia in the upper extremities. .Alternatively, heightened reflexes can be demonstrated by the presence of Hoffmann's sign.

Jaw jerk - A complete guide

Jaw jerk is a deep tendon reflex that help to localise the lesion to above the level  of pons. This is a stretch reflex used to test the status of a patient's trigeminal nerve (CN V).Jaw jerk  is a classic monosynaptic stretch (myotactic) reflex, common to many somatic joints. The jaw jerk reflex can be classified as a dynamic stretch reflex
The jaw jerk reflex was originally described by Lewis in 1882
Other names of jaw jerk
Chin reflex, Chin-jerk reflex, Mandibular reflex. masseter reflex
How to perform jaw jerk?

• Ask the patient to open the Mouth partially and the jaw relaxed
• Tongue remains inside the mouth.
• Left  index finger of the examiner is placed over the middle of the patient's chin.
• The index finger is then tapped with a reflex hammer, delivering a downward stroke.
• The normal response is slight and constists of sudden closure of the mouth.(the masseter muscles will jerk the mandible upwards).

This reflex is sometimes absent in health.
Normal Response:
The jaw should not deviate to either side. The jaw-jerk is usually absent or weakly present.
Abnormal Response:
The jaw deviates towards the side of weakness.
the jaw-jerk is exaggerated and pathologically brisk with lesions affecting the pyramidal pathways above the 5th nerve motor nucleus, especially if the lesions are bilateral.


Clinical significance of jaw jerk
The Jaw jerk is increased In tJMN lesions above the Vth cranial nerve nucleus occur in the following conditions

• Pseudobulbar palsy
• Multiple sclerosis. 

In patients with spastic quadriparesis , an exaggerated jaw jerk excludes cervical cord disease and it points to pyramidal tract disease above the pons .This reflex will help to distinguish an upper cervical cord compression from lesions that are above the foramen magnum.
The mandibular reflex, or jaw jerk, is the only monosynaptic reflex available for electrophysiologic testing in the cranial muscles
How does the jaw jerk reflex help in localizing lesions in patients with hyperreflexia?
The jaw jerk is a reflex that involves the contraction of the masseter and temporalis muscles when the patient's lower jaw is tapped. The jaw jerk is exaggerated with bilateral lesions above the level of trigeminal nerve but will not be affected by lesions below it in the spinal cord. This is helpful in patients who have hyperreflexia in all four limbs  because an exaggerated jaw jerk reflex suggests that the lesion is above the level of the spinal cord (i.e., high brain stem or brain).
Hyper reflexia may be  seen in cervical spondylotic myelopathy can be similar to multiple sclerosis (MS) or amyotrophic lateral sclerosis (ALS), however, a hyperactive jaw reflex suggests the pathology is above the foramen magnum. In other words, a normal jaw jerk reflex points the diagnosis toward cervical spondylotic myelopathy and away from MS or ALS.
Path way for jaw jerk
Both the afferent and efferent fibres are present in the trtgeminal  nerve.The afferent impulse for this reflex is the sensory portion of the trigeminal nerve ie the afferent limb travels via the mandibular branch of the trigeminal nerve
Then reach the mesencephalic nucleus of the trigeminal nerve situated in pons.
The efferent limb arises from the motor nucleus of the trigeminal nerve and also travels via the mandibular branch. The efferent limb is through the motor (V3) branch of the trigeminal nerve.


Factors affecting the reflex
Gender, age

Anal reflex -Clinical significance

Anal reflex is an example of superficial reflex

Method of elicitation of Anal reflex

It is elicited by stroking or pricking the skin and mucous membrane in the perianal region (which is  a noxious or tactile stimulus) and feel the contraction of external anal sphincter  with the finger inserted into the anal canal

Response: Contraction of the external anal sphincter.

The stimulus is detected by the nociceptors in the perineal skin to the pudendal nerve, The response is integrated by the spinal cord sacral segments S2-S4.

Other names of anal reflex

Anal wink, Anocutaneous reflex, Perineal reflex 

Root value  of anal reflex -S3,S4,S5

Clinical significance of anal reflex

Absent reflex :

The absence of anal reflex occur due to  an interruption of the reflex arc, or damage to the spinal cord

1. Lesion of the local reflex arch of S4-S5.

2. Pyramidal lesions.

Pectoral jerk -a localising neurological reflex

Pectoral reflex is an example of deep tendon reflex.

Method of eliciting pectoral reflex

Pectoral reflex is elicited by striking the index finger placed on the inferior part of the pectoralis muscle tendon ,that is  close to the insertion

Innervation  of pectoral reflex

It is innervated by C5. T1 segment of spinal cord

Clinical significance of pectoral reflex

Exaggerated in corticospinal tract lesion above C5

Myelopathy from cervical spondylosis is usually accompanied by hyperreflexia of the upper-extremity deep tendon reflexes .The presence of a hyperactive pectoralis reflex is specific for lesions of the upper cervical spinal cord. Examination of upper-extremity DTRs can also help in planning the appropriate levels for surgical decompression in patients with multilevel spondylosis and myelopathy.

Trapezius jerk -clinical significance

Trapezius jerk is an example of deep tendon reflex
The finger is placed over the trapezius muscle parallel to the spine
Then strike the index linger placed on the trapezius muscle
Slight elevation the shoulder can be seen.There is exaggerated reflex in pyramidal tract lesion
Trapezius Jerk Innervation
Trapezius jerk is supplied by spinal segment C3,C4
Abnormality in Trapezius jerk 
It is exaggerated in corlicospinal tract lesion above C3
Commonly seen in patients with cervical spondylosis
Examination of upper-extremity deep tendon reflex may be helpful in planning the appropriate levels for surgical decompression in patients with multilevel spondylosis and myelopathy

What are the causes of absent of knee jerk ?

Absent knee jerk  signifies the lesion at the level of L4 spinal segment.

• Absence of the knee jerk signify an abnormality anywhere within the reflex arc, including the muscle spindle, the Ia afferent nerve fibers, or the motor neurons to the quadriceps muscle. 
• In general the afferent loop is much more critical for reflex function than the efferent loop, hence that unless the muscle is almost paralysed, loss of reflexes suggests a sensory nerve or root lesion rather than a motor nerve lesion.
• The most common cause is a peripheral neuropathy from such things as diabetes, alcoholism, and toxins.

Causes of absent ankle jerk

• Non-cooperative patient or faulty technique.
• Acute anterior poliomyelitis.
• Peripheral neuropathy.
• Myelopathy in shock stage.
• Progressive musclar atrophy (MND).
• Subacute combined degeneral ion.
• Friedreich's ataxia
• Tabes dorsalis
• Sometimes in diseases of myoneural Junction (myasthenic crisis, hypokalaemia etc).
• Muscular dystrophy in late stages.

If there is  loss of deep reflex restricted to one limb only, you have to rule out the following conditions

• Acute anterior poliomyelitis, 
• Entrapment neuropathy, 
• Leprosy 
• Diabetic mononeuropathy.

Always perform the Jendrassik's manoeuvre before declaring a tendon reflex absent