Central Nervous System Examination PDF

Central Nervous System Examination 4th year B batch Guide: Dr. Jignasha ma'am Glasgow coma scale Higher Functions Consciousness Behaviour Intelligence Memory - past and present Orientation in time, place and person Hallucinations, delusions Speech I. Consciousn...

Central Nervous System Examination 4th year B batch Guide: Dr. Jignasha ma'am Glasgow coma scale Higher Functions Consciousness Behaviour Intelligence Memory - past and present Orientation in time, place and person Hallucinations, delusions Speech I. Consciousness Consciousness is a state of awareness of one's self and one's environment. ❑ Sleep: Sleep is a state of physical and mental inactivity from which the patient can be aroused to normal consciousness. ❑ Catatonia: Catatonia is a state during which rigid plastic postures of limbs for long hours are assumed. The person is unresponsive, mute and immobile. It may occur in psychosis or with frontal lobe and hypothalamic lesions. ❑ Akinetic mutism: Akinetic mutism is a state during which the patient remains immobile, making no sound, follows movements slowly with his eyes and allows himself to be fed and nursed. This is seen with lesions of diencephalon and brainste. ❑ Drowsiness: This is a pathological state that resembles normal sleep. Patient can be aroused with an exernal stimulus, but reverts back to his drowsy state on withdrawal of the stimulus. ❑ Semicoma: Semicoma is a pathological state, which requires stronger stimulation to arouse the patient, though his reflexes are normal. ❑ Stupor: Stupor is often considered synonymous to semicoma, whereas some doctors regard it as a state between drowsiness and semicoma. ❑ Coma: This is the deepest level of unconsciousness. Patient is immobile, all the reflexes are absent and planter response is extensor. II. Delirium Delirium is the acute state of confusion with excitement and hyperactivity. ❑ Causes:- 1. Infective : Septicemia, typhoid, cerebral malaria 2. Withdrawal state: Alcohol 3. Toxic: Overdose of aspirin,amphetamine, atropine, etc. 4. Deficiency of thiamine and nicotinic acid 5. Metabolic : Renal failure, porphyria III. Delusions:- Delusions are false beliefs, which cannot be corrected in spite of evidence to the contrary. Delusions have to be distinguished from superstitions, which are a part of the cultural traditions in ❑Causes:- 1. Holistic: Delusions of disordered or diseased body, e.g., the body is riddled with cancer or his sex is changing. This is seen in schizophrenia or depressive illnesses. 2. Delusions of guilt: Patient may blame himself excessively for some trivial lapse and expect to be imprisoned or hanged for the same. This is seen in depressive states. 3. Delusions of grandeur: e.g. A patient who is a beggar may say that he is the richest man in the world, and is about to marry the Premier's daughter. This is seen in GPI mania and paranoid schizophrenia. IV. Hallucinations This is false perception of sensations in the absence of any sensory stimulus e.g. humming in the ears when there is no sound or seeing somebody who does not exist. This has to be distinguished from illusion, which is altered perception to sensory stimulus, e.g. mirage in the desert. V. Thought Content Sudden onset of fear or depression before an epileptic attack points to temporal lobe origin. Teichopsia preceding an attack of migraine represents occipital visual hallucinations. Grandiose delusions are the hallmark of GPI (Neurosyphilis). VI. Insight Lack of insight is seen in: i. Lesions of frontal lobe ii. With deteriorating intelligence VII. Emotional State Hostile, depressed or euphoric. Whether the emotions are appropriate or not. Causes of lncontinence of emotions/ Emotional lability. i. Pseudobulbar palsy ii. Cerebral arteriosclerosis, multi-infarct state iii. Organic dementia vascular iv. Multiple sclerosis VIII. Memory A. Defect in registration: This is largely due to inattention. It is seen in: C. Defects in recall seen in: 1. Toxic delirium 1. Post traumatic states 2. Manic states 2. Epilepsy 3. Senile dementia 3. Korsakoff's psychosis B. Defects in retention: This is 4. Ganser's syndrome seen in organic cerebral 5. Hysteria disturbances like: 1. GPI 2. Frontal lobe lesion 3. Senile dementia DEMENTIA : Dementia is an acquired deterioration of cognitive abilities. It comes in the way of performing activities of daily living. Memory is most commonly affected Causes of Dementia Treatable/Reversible 1. Drugs/Toxins: Alcohol, narcotic poisoning 2. Vitamin Deficiency: Bl, B 12, B3 (pellagra) 3. Infections: Syphilis, TB 4. Neoplasm: Primary or metastatic brain tumor 5. Trauma: Chronic subdural hematoma, normal pressure hydrocephalus 6. Endocrine: Hypothyroidism, Addison's syndrome, Cushing's syndrome, hyperparathyroidism 7. Miscellaneous: Vasculitis, liver/renal failure Untreatable/ Irreversible 1. Degenerative Diseases: Alzheimer's, Parkinson's, Huntington's disease 2. Infections: HIV, Sub acute Sclerosing Panencephalitis 3. Prion diseases: Creutzfeldt-Jacob disease 4. Multiple sclerosis 5. Multi-infarct dementia NUTRITION Bulk of muscle How to measure : For Upper Limb :- 1. 4 Inches above and below to olecranon process and marked the circumference on both upper limb. 2. In decreased nutrition – The circumference decreased if person is right handed  For lower limb:- 1. Take reference point of tibial tuberosity and measure 6 inches above and below measure circumference. 2. In lower limb there is no natural difference In both limb, as in upper limb the ½ inch difference means wasted. Hypertrophy of Muscles : 1. Mostly seen in large muscle 2. Calf muscle of leg 3. Infraspinatus But these muscle are weak, inspite of their size hence they are called pseudohypertrophy. Wasting of muscle : Poliomyelitis, fracture, muscular dystrophy, any spinal disorder, leprosy, TB, HIV, malignancy etc. Causes : Parietal Lobe Lesions Vertebral Lesions Spinal Cord Lesions Peripheral Nerve Lesions Muscle Disease Disuse Atrophy Systemic Wasting TONE 1. Resistance offered by skeletal muscle during passive movement. 2. Muscular tone is a state of tension or contraction found in healthy muscle. 3. Decreased tone – hypotonia 4. Increased tone – hypertonia 1. Hypotonia : Is characterized by flabby muscle, which offer less resistance to passive movements leading to an increased range of passive movement and the limb is unable to maintain posture. Causes : - Lower motor neurone disease - Cerebellar disease - Rheumatic chorea - Sleep - Drug effect 2. Hypertonia: Is increased resistance to passive movements, a heightened salience of the muscles and increased firmness on palpation. Causes: -Pyramidal disorder -Extrapyramidal disorder -Hyterical -Tetanus -Stiff man syndrome Types: 1. lead pipe rigidity: - There is increased tone, both in flexors and extensors. - The resistance is present throughout the entire range of movement. 2. Cogwheel rigidity: - The increased resistance is throughout the entire range of passive movement and is rhythmically jerky. 3. Decerebrate rigidity: - Marked contraction of all extensor muscle. - The limbs are stiff, extended, head is erect and the jaw is closed. 4. Clasp knife spasticity: - Increased tone in the flexors of upper limb. - The resistance is increased only at the beginning or at the end of passive movement. Power The power of all the muscles should be tested at each joint in both the upper and lower limbs both against gravity and against resistance.  Grading Grade 0 : no power Grade 1 : flicker of contraction only Grade 2 : movement with gravity eliminated Grade 3 : movement against gravity Grade 4 : movement against gravity & some resistance Grade 5 : normal power Ataxia Ataxia= Abnormal gait Abnormality in walking & standing  Causes 1) cerebellar - vascular lesions - enechephalitis - hereditary - drugs, alcohol 2) sensory - peripheral neuritis - partial lobe disorder - posterior column 3) labyrinthine - acute labyrinthitis - meniere's disease TEST - 1) Romberg's test = pt is asked to stand with feets closely. When 1st Eye's open or 2nd close eyes. = In sensory ataxia - pt is able to upright position when eyes are closed & he sways = In cerebellar ataxia - Difficulty in standing when eyes are open. if right side lesions pt fall right side. if central lesions pt fall forward & backward = in hysteria - false Romberg' s sign & marked unstediness.  2) cerebellar Sign - pt is ask to walk in straight line & 1st foot in toe & 2nd foot in heel when touches & perform the close eyes & open eyes. Sensory ataxia= sways on close eyes Cerebellar ataxia= sways on open eyes 3) finger nose test - pt is asked to abduct & extend the arm completely. - The touch the tip of the index finger to tip of the nose. - performed the test slowly then rapidly then again eyes open & closed. = sensory ataxia - unable to find the nose when eyes are closed. = cerebellar ataxia - intention tremors, dysmetria, dyssynergia.  # intention tremors = when you ask person to touch nose, tremors started on beginning of performing the test. # dyssynergia = entire movement are dissorted 4) Finger to finger test - - hands should apart to each other -open eyes - finger to finger touch in cerebellar ataxia can't perform - closed eyes - finger to finger touch In sensory ataxia can't perform  5) dysdiadochokinesia- pt is asked to supinate and pronate alternately. -mismatched between agonist and antagonist.  6) rebound test -pt is asked to flex his arm & shoulder & forearm at elbow ,clench fist firmly.examiner pull on wrist against resistance & suddenly release. In normal - contraction of triceps In cerebellar ataxia - pt is unable to Stop the contraction of the flexor. 7) knee heel test -in supination heel of one leg -shin of tibia form knee to ankle with eyes open or closed Dysmetria dyssynergia distension tremors. Involuntary Movement 1) tremors - regular rhythmic contraction of agonist & antagonist. A. static - present at rest - cause tremor - commonly our in one or both hands, jaw, tongue ex.parkinsonism. B. Action /postural - present when limb is actively maintain in certain position anxiety, Hyperthyroidesm. C. Intension - fully expressed on Performing excesting precise will movement especially when desire object is approached. Ex. Cerebellar disorder D. Hysterical- Tremos any of limb if affected limb is restrained by examiner, It move to anothers part of body. 2. chorea:- involuntary movements which are quick, brief, sudden, jerty, irregular in Time , rhythm, character, place of occurrence Cause= infection, liver disease, hyperparathyrodism , porphyria, Drugs -l-dopa, lithium etc. 3. athetosis - involuntary movement slow rhythmic more distally than proximal. Cause - congenital, birth injury, infections , atherosclerosis, l dopa over doses , metabolic disorder , cerebral palsy. 4) tics- involuntary stereotypes movement. types - 1) vocal tics - simple & complex 2) motor tics - clonic &dystonic  Sensory System 1) Touch : ‘Von frey’s hair aesthesiometer ▪ Starts from leg ▪ Touch the areas which are exposed ▪ eyes close ▪ Do not grasp pt’s hand ▪ Only touch by cotton ▪ Ask pt to say yes or no if helshe felt it [can be done by blunt portion of pin] 2) Pain : ▪ Superficial/cutaneous pain ▪ Deep/Pressure pain Superficial - By pointed needle (gentaly) (it means if pain so say yes otherwise say no) Deep - Squeeze the calf muscle - knuckle – compress over sternum If pain absent – analgesia If pain threshold reduce - Hypoalgesia Small amount of pain – Hyperalgesia feel too much Claves Tender – In peripheral neuritis 3) Temperature:- 2-Testtube : 1) Luke warm water 2) Cold water Site – on forearm & dorsum of hand & forearm 4) Position :- Joint position 1st – great toe than other By joint continue movement – dorsiflexion & planter flexion ⇩ 2 to 3 time karvani ⇩ Fix the toe & ask person where is toe? or ask to do same on other leg. 5) Vibration :- the foot of vibrating tunning-fork is placed on the surface of the body the vibration can be felt vibration lost in diseases, as in tabs dorsalis, In peripheral neuropathies and in posterior column disorders. If the patient perceives the vibration, as it gradually fades in intensity, ask them to say when they cease to feel it. If the examiner can then still perceive it, the patient’s perception of vibration is impaired  Cortical sensation 1) Tactile localisation – Ask the person to localise the area by finger with eyes close α. Tactile discrimination- every facet has 2 pin. - Discriminate distance between 2 pin - Dermatones are too near so we can not able to distinguish between one or 2 - In normal person also we can not discriminate α. Tactile extinction: Person has to identify that local point on other side of body Stereognosis- By touch pt has to identify the object & object should be familiar one. Signs of meningeal irritation: Kernig’s sign- In supine position 90° flexion of hip & flexion of knee ⇨ In patient with meningeal irritation affecting the lower part of spinal subarachnoid this movement cause pain and spasm of hamstrings extension. Brudzinsla’s sign: Passive flexion of neck by palm Flexion of hip and knee. Reflexes Superficial Reflexes Planter reflex (S1) Abdominal reflex (T7 – T12) Cremasteric reflex (L1) Bulbocavernous reflex (S2- S4) Anal reflex (S4-S5) Hoffmann’S sign  Planter reflex(S1) Normally – flexor Response On stroking the lateral Border of The sole , there is Flexion of the big toe and all the toes Extensor planter response- Fanning of the Small toes Dorsiflexion of the big toe Dorsiflexion of The ankle Contraction of tensor fascia data Flexion of knee and hip Absent planter reflex- Loss Of sensation of The sole Paralysis of Extensor hallusis Thick planter skin Cauda equinA lesion Lesion of first sacral Segment Causes – Pyramidal lesion Deep sleep or coma IN infantS it is normally present hypoglycEmia post seizure Abdominal reflex (T7- T12) Elicited by Gentle stroking OF abdomen with blunt object response Homolateral Contraction of abdominal muscles And retraction of linea alba And umbilicus towards the area stimulated Absent Marked obesity and abdominal distension Multiparous women with lax Abdomen Lesion of local reflex arch Of T7-T12 Typhoid perforation Post abdominal surgery  Cremasteric reflex ( L1) Elicited by Stroking the skin On upper ,inner aspect of thigh From above downward With a blunt point Response Contraction of cremasteric Muscle With homolateral Elevation of testicle Absent Lesions of local reflex arch Of L2 Pyramidal Lesions Hydrocele Hernia  Bulbocavernosus Reflex (S2- S4) Elicited by pressing glans penis Response Contraction of bulbocavernosus muscle Felt at the junction of Penis and scrotum Absent Lesion of local reflex arch of S2-S4 Pyramidal lesions  Anal reflex (S4- S5) Elicited by Stroking or Pricking the skin On mucus membrane In the perianal region Response Contraction of The external anal sphincter Absent Lesion of The local reflex arch Of S4-S5 Pyramidal lesionS  Hoffmann‘s sign Method The patient‘s hand Is pronated And observer grasps the Terminal phalAnx of middle Finger between His forearm and thumb With the sharp Flick, Phalanx is passively Flexed and suddenly released A positive response Consist of Sharp Twitch With adduction And flexion of Thumb and flexion of fingers  Significance It is An index of Muscular hypertonia Rather than of Pyramidal lesion As such It is not always positive In presence of Pyramidal lesion It may be elicitable In a nervous individual With no organic Disease If it is present one side only, it is likely to be significant  Deep reflex 1) Biceps reflex (c5-c6). 2) Triceps (C7-c8) 3) supiNator (c5-c6) 4) Finger flexion (c7-c8) 5) Knee reflex. (L3-l4) 6) Ankle reflex (S1-s2)  Nerve- musculo cutaneous nerve Bicep tendon is not visible so place the thumb of examiner in medially of elbow. Elbow flexed at 90°.put thumb on biceps tendon & strike the broad end of Hammer to prevent injury to bicерs. Visible contraction of muscle on arm occur.(Flexion of elbow). Absent : Stroke LMN disorder. Bruin trauma Meningitis. spinal cord injury Triceps reflex Nerve-Radial nerve Elbow flexed at 90° Tendon is visible so no need to put thumb arm relaxed & Strick the tendon with Broade end of Hammer. Extension /contruction of triceps(arm). Supinator reflex Nerve-Radial nerve Blow upon tendon of brachioradialis at distal end of the radius. Flexion of forearm with supination.  Finger flexion Nerve-Median and ulnar nerve Patients hand is supine with fingers relaxed and slightly flexed. Examiner’s fingers are placed over the proximal part of the patients fingers and he strikes them with hammer. Normally there is slight flexion of fingers. Flexion of the finger and thumb. Positive: brisk flexion of all fingers indicating a lesion of C6 – T1. Knee reflex Nerve-Femoral nerve Sitting with cross leg Strick bony part with broad end of hummer Extension of knee joint.  ANKLE REFLEX Nerve-sciatic nerve always done in supine position in supine knee should be fiexed and put one leg on another leg flexion of ankie stick on tendoachilis with broad end of hammer Cranial Nerves 1st cranial nerve : olfactory nerve It belongs to special visceral afferent column.  Receptors and 1st neuron : 1. olfactory cells 2. Olfactory nerves 2nd neuron : olfactory bulb gives off the fibres that forms olfactory tract and reach primary olfactory areas. 3rd neuron : located in primary olfactory cortex which includes anterior perforated substance and small masses of grey matter.  4th neuron : Fibres arising in the primary olfactory cortex go to the secondary olfactory cortex located in uncus and anterior part of parahippocampal gyrus. Smell is perceived both in primary and secondary areas. Olfactory Pathway Olfactory epithelium of nose olfactory rootlets olfactory bulb lateral and medial olfactory striae Lateral olfactory striae pyriform lobe Medial olfactory striae septal nuclei Olfactory Function Test Interpretation of test Normal : recognize name and odour quickly. Recognize but cannot name them. Can detect smell and easily distinguish differences , but can neither recognize nor name them. Degree of smell aberration : Anosmia - absence of smell sensation Hyposmia - diminished sense of smell Parosmia - perverted sense of smell Cacosmia - perception of unpleasant odour in absence of olfactory stimuli  Hyperosmia - acute sense of smell Presbyosmia - decrease sense of smell due to aging Coprosmia - cacosmia with fecal sent Phantosmia - perception of smell that is not real  Causes Of Anosmia : nasal polyp , viral URTI , rhinitis , head trauma , meningitis , heaheavy smoking , radiation , zinc deficiency , subarachnoid haemorrhage , parkinson's disease , hysteria  2nd cranial nerve : optic nerve Embryology: Optic nerve head is formed in late embryonic period as optic stalk encloses the hyloid artery (8th week) Physiological cupping develops at 15th week. Optic nerve develops from embryonic optic stalk (4th week ) and connects optic vesicle to fore brain. As the stalks lengthens, nerve becomes thinner and is progressively occupied by axons growing from ganglion cell layer. Myelination begins centrally, progresses in centrifugal direction. Myelination is completed shortly after birth. Parts of optic nerve Intra ocular part Intra orbital part Intra canaliculi part Intra cranial part Blood supply Pupillary reflexe Light reflex : When light is shown to one eye.. Both pupils constrict Direct vs consensual Almost identical in time, course & magnitude If both pupils iluminated at once-> summation Dependant the state of adaptation of the retina, emotions, alertness Maximum frequency of stimuli is 5 Hz  Initiated by retinal photoreceptors Transmitted along optic nerve Undergo a hemidecussation at the optic chiasma(nasal fibres cross over) Proceeds along optic tract Synapses at pre- tectal nucleus Ends in both Edinger westpal nucleui Any given pretectal neuron behaves functionally as though it recieves similar inputs from each eye & projects equally in each EW nucleus Ipsilateral-> around periaqueduct Contralateral-> via the posterior commissure  Efferent fibers travel on the surface of CN-Ill to inf. Obl. &/ due to long course-> unilateral defecits can be of localizing significance in unilateral pathology Synapse & relay at ciliary ganglion Post ganglionic fibres reach ciliary muscle and iris spincter through short ciliary nerves to reach the sphincter pupillae Cerebral cortex sends inhibitory signals to EW nucleus-> absence leads to meiosis during sleep Functions: Protects against excessive bleaching of the visual pigments Light/Dark adaptation to maximize VA  Corneal reflex is an involuntary blinking of the eyelids elicited by stimulation of the cornea (such as by touching with cotton or by a foreign body), though could result from any peripheral stimulus. Stimulus: touch by cotton Stimulation should elicit both a direct and consensual response Significance: protect the eyes from foreign bodies and bright lights. Responsible nerve: 5th cranial nerve (trigeminal nerve) Afferent arc is mediated by the nasociliary branch of the ophthalmic branch (Vi) of the trigeminal.  Center: in the pons of brain stem Efferent arc is the seventh (facial) nerve mainly temporal branch. Effector organ: orbicularis oculi Procedure: take a wisp of cotton then ask the patient to look straight ahead. Gently, brush the cotton against sclera or cornea, this will make the patient blink. An abnormal corneal reflex may indicate either fifth nerve afferent disease or seventh nerve efferent disease or tolerance. Oculomotor Nerve The nucleus for the third cranial nerve is in the midbrain. The nerve emerges ventrally (anteriorly), medial to the cerebral peduncle, passing forward through the cavernous sinus to the superior orbital fissure. In the orbit, the superior ramus sup- plies superior rectus and levator palpebrae superioris. The inferior ramus supplies inferior rectus, inferior oblique and medial rectus, and parasympathetic fibres from the inferior ramus pass to the ciliary ganglion and thence to the ciliary muscle and the pupil sphincter FUNCTION OF OCULOMOTOR NERVE Have your upper eyelid raised. Bring your vision focus. Pupils constrict in response to illumination, allowing more light into the eye. It is possible to manage torsion by directing the gaze inwards, outwards, and downwards. Lesion Of The Oculomotor Nerve Ptosis: paresis of the levator palpebrea superior muscule. Diplopia: occurs only on elevation of eye lid. Squint: divergent paralytic. Mydriasis: dilated fixed pupil. Loss of light and accommodation reflexes.  DIEASES OF OCULOMOTOR NERVE ￭Brain tumor: ￭Head injuries: ￭Brain aneurysm: ￭Atypical head motions:  IV – TROCHLEAR NEARVE ORIGIN: Midbrain INNERVATION: superior oblique muscle. FUNCTION: Down and inward movement of the eye. DYSFUNCTION: Loss of downward, inner movement of eye, dysconjugate. VI – ABDUCENS NERVE ORIGIN: Pons INNERVATION: Lateral rectus muscle. FUNCTION: Outward, lateral movement of eye. DYSFUNCTUON: Loss of lateral eye movement, dysconjugate gaze.  TYOE OF SIXTH NERVE PALSY Sixth Nerve Palsy Total palsy Partial palsy (paralysis) Cause of Third Nerve Lesion 1. Posterior communicating artery aneurysm. Carotid artery aneurysm. 2.Neoplasm at the base of the skull, sphenoidal wing or parasellar. 3. Upper midbrain vascular accidents. 4. Demyelinating lesions Cause Fourth Nerve Lesion and Sixth Nerve Lesion Cerebral peduncle lesion Raised intracranial tension Fifth Cranial nerve Fifth cranial nerve also known as Trigeminal nerve. It is the largest canial nerve. Its name derives from each of the two nerves (one on each side of the pons) having three major branches: the ophthalmic nerve (V1), the maxillary nerve (V2), and the mandibular nerve (V3). The ophthalmic and maxillary nerves are purely sensory, whereas the mandibular nerve supplies motor as well as sensory functions. Anatomy Origin From the trigeminal ganglioThe three major branches of the trigeminal nerve—the ophthalmic nerve (V1), the maxillary nerve (V2) and the mandibular nerve (V3)—converge on the trigeminal ganglion (also called the semilunar ganglion or gasserian ganglion), located within Meckel’s cave.  Ophthalmic Nerve Division Ophthalmic Nerve is sensory. It’s branches are : Frontal :- 1. Supratrochlear: Upper eyelid, conjunctiva and lower part of forehead. 2. Supraorbital: Frontal sinus, upper eyelid, forehead and scalp till vertex.  Nasociliary:- 1.Long ciliary: sensory to eyeballs 2. Posterior ethmoidal : Sphenoidal air sinus , posterior ethmoidal air sinuses. 3. Anterior ethmoidal: Middle and anterior ethmoidal sinuses, medial internal nasal, lateral internal nasal, external nasal. 4. Infratrochlear : Both eyelid , side of nose, lacrimal sac.  Maxillary nerve division It is sensory and branches as below: 1.In Middle cranial fossa: Meningeal branch 2. In Pterygopalatine fossa: zygomaticotemporal, Zygomaticofacial, posterior superior alveolar. 3. In Infraorbital Canal: Middle Superior alveolar, Anterior superior alveolar 4.On face: Infraorbital, Labial, nasal.  Mandibular nerve division It is mixed nerve and it’s branches are: 1.From Trunk: Meningeal, nerve to medial pterygoid. 2. From anterior division: Deep temporal, Lateral pterygoid, Masseteric, Buccal skin of cheek. 3. From posterior division: Auriculotemporal , Lingual – general sensation from anterior two –third of tongue, lower teeth, inferior alveolar. Examination Sensory:- 1. Tell the patient you are going to test the ability to feel touch or pain on the face. The eyes should be close. Take a piece of cotton or the ball of your finger. Lightly touch either one or both sides of each of the three divisions of the trigeminal. Ask the patient to show or say whether you touched one or both sides of the face. 2. Take a safety pin and gently prick first one side of each division and then the other, asking the patient if there is any difference in the sensation on one side compared to the other. With the patient’s eyes closed, touch sometimes with the sharp point of the pin and at other times with the dull guard. Ask the patient to describe the sensation. 3. Test the corneal reflex. Begin by telling the patient you are going to touch the eye gently in order to check the reflex. Take a wisp of cotton and twist it into a point. Ask the patient to look in the other direction, so you will not be testing the blink reflex. Then gently but firmly touch the cornea at its junction with the sclera. Sensitivity to pain increases medially from this point and decreases laterally. The junction of the cornea and sclera is a good compromise between causing pain to the patient and obtaining the reflex. There is a rapid blink of the eye being tested and a consensual blink of the other eye. If there is seventh nerve weakness on the side being tested, then observe the consensual reflex.  Motor 1. Ask the patient to clench his or her jaws. Palpate the masseter and temporal muscles for asymmetry of volume and for tone. 2. Observe the skin over the temporal masseter muscles. Concavity or asymmetry suggests atrophy. The tip of the mandible should be in the midline.  Seventh Cranial nerve Seventh Cranial nerve also known as facial nerve. Anatomy:- The motor part of the facial nerve arises from the facial nerve nucleus in the pons, while the sensory and parasympathetic parts of the facial nerve arise from the intermediate nerve. Intracranial branches: provides parasympathetic innervation to several glands, including the nasal glands, the palatine glands, the lacrimal gland, and the pharyngeal gland. It also provides parasympathetic innervation to the sphenoid sinus, frontal sinus, maxillary sinus, ethmoid sinus, and nasal cavity. This nerve also includes taste fibers for the palate via the lesser palatine nerve and greater palatine nerve. Extracranial branches: Posterior auricular nerve which controls movements of some of the scalp muscles around the ear. Branch to posterior belly of digastric muscle. Branch of the stylohyoid muscle. Five major facial branches (at parotid plexus) – from superior to inferior: Temporal branch Zygomatic branch Buccal branch Marginal mandibular branch Cervical branch Function:- Responsible for muscles of facial expression and elevation of hyoid bone. Carries afferent impulses from above mentioned glands. Carry tastes sensation from the palate and from anterior two – third of the tongue except from vallate papillae. The nerve does not give any direct branches to ear but some fibers may reach it through communication with the vagus nerve. Parasympathetic fibers secretomotor to the submandibular and sublingual salivary gland, lacrimal glang, gland of the nose, palate and pharynx. Examination:- Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called lagophthalmos),pursing the lips and puffing out the cheeks, all test the facial nerve. There should be no noticeable asymmetry. Taste can be tested on the anterior two-thirds of the tongue. This can be tested with a swab dipped in a flavoured solution. The corneal reflex effectively tests the proper functioning of both cranial nerves V and VII.  Eighth Cranial Nerve It also known as Vestibulocochlear nerve. Anatomy:- The vestibulocochlear nerve consists mostly of bipolar neurons and splits into two large divisions: the cochlear nerve and the vestibular nerve. The cochlear nerve travels away from the cochlea of the inner ear where it starts as the spiral ganglia. The vestibular nerve travels from the vestibular system of the inner ear. The vestibular ganglion houses the cell bodies of the bipolar neurons and extends processes to five sensory organs. Function:- This is the nerve along which the sensory cells (the hair cells) of the inner ear transmit information to the brain. It consists of the cochlear nerve, carrying details about hearing. The vestibular nerve, carrying information about balance. It emerges from the pontomedullary junction and exits the inner skull via the internal acoustic meatus in the temporal bone. Clinicals:- Deafness: Conductive deafness, Sensorineural deafness, Cortical deafness. Vertigo. Tinnitis. Meniere’s syndrome. Acostic neuroma. Examination:- Examinations that can be done include the Rinne and Weber tests. If bone conduction (BC) is more than air conduction (AC) (BC>AC) indicates Rinne Test is negative or abnormal. If AC>BC Rinne test is normal or positive. If BC>AC and Weber’s test lateralizes to abnormal side then it is Conductive hearing loss. If AC>BC and Weber’s test lateralizes to normal side then it concludes Sensorineural hearing loss. CRANIAL NINTH,TENTH AND ELEVENTH NERVES  ANATOMY The ninth, tenth and eleventh nervers arise in that order from above downwards, in an elongated nucleus in the floor of the fourth ventricle. They emerge along the lateral aspect of the medulla.  The spinal part of eleventh nerve (accessory) from the lateral columns of the spinal cord passes up through the foramen magnum and joins the cranial part of the accessory nerve and emerges with it through the jugular foramen. The ninth (glossopharyngeal) nerve supplies the sensation including the taste sensation to the posterior one-third of the pharynx. It also supplies the middle constrictor of the pharynx and stylopharyngeus muscle. The tenth(vagus) nerve is motor for soft palate(except tensor palati), pharynx and larynx. It is sensory and motor for the respiratory passages, the heart and the abdominal viscera.  The eleventh (accessory) nerve is a pure motor nerve for innervation of the larynx, pharynx, sternomastoid and trapezius muscles.  TESTS The sensory part can be tested by testing the superficial as well as the taste sensation over the posterior one third of the tongue. The motor function is tested as follows: 1. The patient is asked to open the mouth and say “ah” and palatal movements on both the sides are noted. Normally they are equal and uvula is in the centre. In unilateral palatal palsy, the median raphe is pulled to the normal side, as palatal movements on the affected side are absent. In bilateral paralysis, the whole palate remains motionless. 2. The trapezius muscle is tested by asking the patient to shrug his shoulders against downward resistance. Normally both the sides are equal. In unilateral paralysis, there will be weakness on the affected side. 3. The sternomastoid muscle is tested by asking the patient to rotate his chin to the opposite side. In unilateral paralysis, the chin is deviated to the affected side and there is impairment of rotation of the chin to the opposite side.  The reflex function is tested by examining the gag reflex.  Gag Reflex Reflex centre: Medulla Efferent: Vagus Method: Stimulation of the posterior pharyngeal wall by a tongue blade or a cotton applicator results in elevation and constriction of the pharyngeal musculature accompanied by retraction of the tongue. Significance 1. The reflex may be absent or brisk in hysteria 2. The reflex is lost in lessions of the IX and X nerves.  Cranial Twelfth Nerve Anatomy: The twelfth (hypoglossal) nerve arises from the hypoglossal nucleus in the floor of the fourth ventricle in the medulla oblongata. The fibers of the hypoglossal nerve emerge medial to the fibers of glossopharyngeal nerve and unite into two bundles that pass separately through the dura mater and the hypoglossal canal of the skull. After leaving the skull the two bundles unite and pass in the neck and then to the tongue to which it supplies the motor branches.  The supranuclear control is through the corticobulbar fibers. The genioglossus is controlled by contralateral corticobulbar tracts whereas the other muscles have a bilateral supranuclear control. Tests: The tongue should be observed at the rest and on protrusion and various movements are noted. Unilateral lesion may cause paresis, atrophy, furrowing, fibrillation and fasciculation on the affected half of the tongue. On protrusion, the tongue deviates to the paralyzed side due to unopposed action of the contralateral genioglossus. Bilateral weakness in addition, causes dysphagia and dyspnea when the flaccid tongue falls back and obstructs the pharynx. Dysarthria especially for d and t phonemes occur. Thank You