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Nervous examination in small animal

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Nervous examination in small animal by Dr. Kanwarpal Singh Dhillon

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Nervous examination in small animal

  1. 1. Neurological examination and neurological manifestation in systemic diseases in small animals Submitted by: Dr. KANWARPAL DHILLON M.V.Sc – Medicine GADVASU,LDH
  2. 2. Neuroanatomy cerebrum cerebellum Spinal cord Medulla oblongata Sciatic nerve Femoral nerve Radial nerve
  3. 3. The objective of the neurological examination is…. 1. To determine the presence or absence of nervous system malfunction. 2. To establish location of lesion within the nervous system. 3. To arrive at diagnoses. 4. To predict prognosis of disease.
  4. 4. History  It is very important to take a thorough history as this can give many clues in making the most likely differential diagnoses.  species, breed, sex and age of animals.  carefully question owners about the main complaint.  The onset, evolution and course of the illness are most important for making the most likely differential diagnoses.
  5. 5.  The onset of the neurological signs should be defined as: 1. Acute (onset over minutes to hours) 2. Subacute (onset over days) 3. Chronic (onset over several days, weeks or months) 4. Episodic (the patient returns to normal between the episodes)
  6. 6. Neurological examination  The neurological examination should be performed in animals that are not sedated, have not received any analgesia or are recovering from seizures or general anaesthesia.  Method of examination : Hands off examination and Hands on examination
  7. 7.  Hands off examination  This part of the neurological examination can be performed while collecting the history. The patient should be left to explore the examination room. The clinician can observe the awareness, mental status, behaviour, posture and gait in an undisturbed manner.
  8. 8.  Mental status: Consciousness, awareness, behaviour  State of consciousness is classified in order of severity as lethargy, depression, obtundation, stupor (semicoma) and coma.  Generally if there is an altered state of consciousness then the lesion is affecting either diffusely both cerebral hemispheres or focally the ascending reticular activating system (ARAS) of the brainstem.
  9. 9.  Consciousness:  Normal- alert, with a normal response to environmental stimuli  Confused and delirious- responding to environmental stimuli in an inappropriate manner  Depressed- drowsiness, inattention and less responsive to environmental stimuli, due to cerebral cortex lesions.
  10. 10.  Stuporous- state of consciousness with reduced response to external stimuli, but can be aroused by a painful stimuli, associated with partial disconnection of reticular formation and cerebral cortex, as in diffuse cerebral edema with compression of the brain stem.  Coma- state of unconsciousness with absence of response to any environmental stimuli including pain, most common cause in small animal is acute head injury with heamorrhage in the pons and midbrain.
  11. 11.  Changes in the patient’s level of awareness and behaviour include disorientation, delirium, aggression, compulsive walking, loss of learned behaviour (e.g. in-house urination, defecation etc.), vocalising and head pressing. Hemi-neglect or hemi-inattention syndrome is the abnormal behaviour in animals with forebrain lesions. The lesion in the forebrain is contralateral to the apparently “ignored” side by the animal.
  12. 12. Hemi-inattention syndrome
  13. 13. Posture and body position  Head tilt - abnormal posture of the head when one ear is lower compared to the other one. A head tilt indicates a vestibular disorder (central or peripheral).  Head turn - Characterized by the posture when the nose and often whole body (pleurothotonus) are turned to one side and ears are at the same median plane. This is most commonly associated with an ipsilateral forebrain lesion.  Ventroflexion of the head – commonly associated with a neuromuscular disorder or spinalcord grey matter lesion.
  14. 14. Head tilt Head turn
  15. 15. Spinal curvature a) Scolisosis (lateral deviation of the spine) b) Lordosis (ventral curvature of the spine) c) Kyphosis (dorsal curvature of the spine) d) Torticollis (twisting of the neck)
  16. 16.  Decerebrate rigidity - a posture when the patient is recumbent and has extension of all limbs and opithotonus (extension of the neck and head). The mental status is often stuporous or comatous and the lesion is commonly localised in the rostral brainstem.
  17. 17.  Decerebellate posture - a posture when the patient is recumbent, has extended thoracic limbs and opisthotonus but the pelvic limbs are usually flexed. The mental status is normal and the lesion is likely to occur in the cerebellum.
  18. 18.  Schiff-Scherrington posture - observed in animals with severe thoracic or cranial lumbar spinal cord trauma. The animal has extended thoracic limbs with the normal function but has paralysis of the pelvic limbs. This sign is present only in acute lesions and does not have any prognostic value.
  19. 19. Evaluation of gait  Ataxia means uncoordinated gait. Ataxia can be a consequence of peripheral nerve or spinal cord dysfunction (general proprioceptive ataxia), vestibular system (vestibular ataxia) or cerebellum (cerebellar ataxia).  Paresis is defined as a loss of ability to support weight or to generate the gait. Monoparesis, paraparesis, tetraparasis,or hemiparesis.  Plegia or paralysis refers to the complete loss of a voluntary movement, whereas paresis implies that the voluntary movements are still present.
  20. 20.  Circling: circling may vary from a tendency to drift in wide circle to forced spinning in a tight circle.  tight circle: lesion in brain stem, direction always towards the side of the lesion  Dysmetria: characterized by movements too long (hypermetria) or too short( hypometria). ‘goose-stepping’ is most common sign of dysmetria. Occur due to lesion in cerebellar and cerebellar pathways.
  21. 21. Abnormal movements: tremor and myoclonus  Tremors- synchronous involuntary oscillating contraction of antagonistic muscle groups. Can affect all or parts of body.  Classified as  Resting tremors  Intention tremors -occur as the animal intend to move and are exaggerated by action oriented movements e.g. eating.  Action tremors (occur as the parts of body are maintained in certain position)  Generalized tremors are more common
  22. 22.  Epileptic seizures- clinical manifestation of excessive or hypersynchronous electrical activity in the cerebral cortex. Can be focal or generalized Occurs due to a fore brain disorder (may be from inside or outside of brain)  Myoclonus- Repetitive rhythmic contraction of a group of skeletal muscles producing a quick jerking movement of a body part. Can be a result of encephalitis or myelitis caused by distemper virus.
  23. 23.  Myotonia- Sustained irregular contraction with delayed relaxation of a muscle or a group of muscles following voluntary contraction.  Cataplexy- Paroxysmal onset of flaccid paralysis with preservation of consciousness lasting for few seconds to few minutes Induced by excitement and can be reversed by an external stimuli  Head ‘bobbing’- Occurs in particular breeds such as bulldog and Doberman pinscher
  24. 24. Hands on examination  Cranial nerve examination  Olfactory Nerve – (CN I)  The olfactory nerve is the sensory path for the conscious perception of the smell.  The behavioral response to a pleasurable or a noxious odor, either inferred from the history or assessed by direct testing by Alcohol, cloves, xylol, benzol, or cat food containing fish, appears to stimulate the olfactory nerves.
  25. 25.  Letting the animal to sniff something aromatic while blindfolded can test the smell response.  Abnormal: Hyposomia or Ansomia
  26. 26.  Optic Nerve (CN II)  Menace response is a cortically mediated blink produced by a threating gesture in front of the visual area of the patient. Puppies will not have this response prior to 10-12 weeks of age.  Pupillary light reflex (PLR) induces by shinning the light in each eye and observing the pupillary constriction in both eyes.
  27. 27. The menace response is performed by making the threating gesture at the eye. The contralateral eye should be blinded. Care must be taken not to touch the eyelashes or to create air current as this stimulates the CNV and produces the palpebral or corneal reflex rather then genuine menace response.
  28. 28.  Oculomotor Nerve (CN III)  This nerve innervates ipsilateral dorsal, ventral and medial recti muscles and ventral oblique muscle. It also innervates the levator palpebrae superioris muscle which is important for upper eyelid movement,  the oculomotor nerve plays an important role as an efferent arm of PLR. It controls the pupillary constriction by its parasympathetic component.
  29. 29.  By observing the eyeball position and movement of the eyeball by testing for physiological nystagmus, this nerve can be easily assessed. Another observation needs to be done by assessing the normal position of the upper eyelid. PLR of course must be assessed.
  30. 30.  An oculomotor nerve lesion results in ventrolateral strabismus and an inability to rotate the eye dorsally, ventrally and medially. It can also produce unresponsive mydriasis and narrowing of the palpebral fissure (ptosis of the upper eyelid).
  31. 31.  Trochlear nerve (CN IV)  This is assessed by observing the position of the eyeball as well as by testing for physiological nystagmus.  This nerve innervates contralateral dorsal oblique muscle.  Dysfunction usually results in dorsolateral strabismus of the contralateral eye.
  32. 32. Dorsolateral strabismus
  33. 33.  Trigeminal nerve (CN V) The trigeminal nerve provides sensory innervation of the face as well as motor innervation of the masticatory muscles. It has three major branches:  1. Ophthalmic branch – innervates medial canthus of the eye, nasal septum, cornea and dorsum of the nose.  2. Maxillary branch – innervates lateral canthus, skin of cheeks, muzzle, palate and teeth of the upper jaw.  3. Mandibular branch – innervates mandibular area of the oral cavity.
  34. 34.  The motor function is assessed by evaluating the symmetry and size of the masticatory muscles as well as by opening the jaw.  The sensory functions assessed by corneal reflex which is done by touching the cornea with a sterile cotton bud. The palpebral reflex tests ophthalmic and maxillary branches (afferent arm of the reflex) by touching medial or lateral canthuses, respectively. A normal response for corneal and palpebral reflex is the blink of the tested eye that is mediated by the facial nerve (efferent arm of the reflex).  Other tests that can assess the trigeminal nerve are nasal stimulation and pinching of the skin of the face that results in the ipsilateral blink or twitch of the facial muscles
  35. 35. palpebral reflex response to nasal mucosal stimulation opening the jaw
  36. 36.  Unilateral dysfunction of the motor part results in unilateral masticatory muscle wastage, whereas bilateral dysfunction results in the dropped jaw and inability to close the jaw voluntarily. Dysfunction of the sensory part results in facial hypoesthesia or anaesthesia and can also result in decreased tear production and neurotropic keratitis. Unilateral wastage of the masseter and temporal muscles
  37. 37.  Abducent nerve (CN VI)  This nerve innervates the ipsilateral lateral rectus and retractor bulbi muscles. The assessment is therefore done by observation of the eye position.  Dysfunction results in ipsilateral convergent strabismus, inability of the eye to cross the midline when testing physiological nystagmus and inability to retract the eyeball. Ipsilateral convergent strabismus
  38. 38.  Facial nerve (CN VII)  The motor function is assessed by observation of the symmetry of the face and spontaneous blink and movement of the nostrils.  The facial nerve provides the efferent arm for palpebral reflex, corneal reflexes and menace response and can be assessed by performing these tests.  The Schirmer tear test should be performed to assess the parasympathetic part of this nerve.
  39. 39.  Unilateral dysfunction produces the ipsilateral drooping of the face, inability to move the ear and nostril, widened palpebral fissure and absent blinking response. It can also produce keratoconjunctivitis sicca by inability to produce enough tears by loss of parasympathetic innervation to the lacrimal glands. Right side dropping of the lips and ear
  40. 40.  Vestibulocochlear nerve (CN VIII)  Observation of the gait, body and head posture can give a lot of information about the vestibular function  Specifically physiological nystagmus can test the functional integrity of the vestibular system.  This involves moving the head from side to side and up and down. A normal response is the involuntary “jerk” movement of both eyes to correct their position in relation to the position of the head.
  41. 41.  To assess the hearing part whistling or a handclap can be use  Dysfunction of this nerve usually results in a head tilt, falling to the side, leaning to the side, rolling, circling, pathological (abnormal) spontaneous or positional nystagmus, positional strabismus or asymmetrical ataxia.
  42. 42.  Glossopharyngeal nerve (CN IX) and Vagus nerve (CN X)  The pharyngeal or gag reflex can assess the function of both nerves. Gently applying pressure to the thyroid cartilages provokes swallowing in a normal animal. Observing a patient while eating or drinking can also provide useful information about the function of both nerves.  Dysfunction results in dysphagia, absent gag reflex, inspiratory dyspnea (due to laryngeal paralysis), voice change and regurgitation (due to megaoesophagus).
  43. 43. pharyngeal or gag reflex
  44. 44.  Accessory nerve (CN XI)  This nerve supplies motor innervation to the trapezius, sternocephalicus and brachiocephalicus muscles and so the dysfunction results in atrophy of these muscles and potential deviation of the neck. However isolated lesions of this nerve are rare.
  45. 45.  Hypoglossal nerve (CN XII)  Assessed by observing for symmetry of the tongue and movement of the tongue during the eating, or licking of food. Lesions of this nerve result in problems with prehension and mastication. Asymmetry of the tongue and fasciculation of the musculature of the tongue can also be seen in dysfunction of nerve.
  46. 46. nerve Diagnostic sign of dysfunction tests Normal responce Abnormal responce I.Olfactory Hyposmia or anosmia Smell of food and voletile oil Food- interested or attempt to eat, voletile oil-sniffing and recolling No reaction II. optic Hesitant walking , walks in to objectes, anisocoria, mydriasis, miosis Sudden object movement towards eyes, Point source of light in each eye Ophthalmoscopy examination Avoidance and eye blink Direct and consensual pupilary constriction Normal fundus Absence of blink reflex Lack of pupillary response Retinal lesion found III.Oculomotor Anisocoria, mydriasis, miosis, ptosis, deviation, ventral and lateral Light in normal eye and light in affected eye Direct and consensual reflex present Direct pupillary reflex present- consensua absent, Direct pupillary reflex absent- consensua reflex may present
  47. 47. IVTrochlear Affected eye anable to move ventrolaterally Observation when animal follows moving objects Follows object ventrolaterally Eye unable to Follows object ventrolaterally V. Trigeminal Sensory- hyperesthesia on one side of face and eye Anesthesia on one side of face and eye Motor-weakness in closing mouth and unable to open mouth Cold object on skin,pinprick.touch cornea Cold object on skin,pinprick.touch cornea Test muscle tension,palpate tempolaris and masseter muscle Slight discomfort ,eye blink both side Slight discomfort Normal muscle tension and normal contour to musculature Intense discomfort, recoil, may vocalize No response Atrophy of temporalis and masseter muscle.trismus VI. Abducens Affected eye unable to move laterally.medial strabismus may present Observation of movment of eye when animal follows moving objects Unable to follow laterally
  48. 48. VII. Facial Asymmetry of facial expression. Eyelids and lips drops.loss of ear motion Observation, pinprick on the side of the face(trigeminal is sensory inthis test) Retractionl of skin eye blink No retraction no eye blink VIII. Acoustic Cochlear nerve-deafness, will not respond to sound Vestibular nerve- circling, head tilt, nystagmus, loss of balance Sudden loud noise, EEG alterting response test Observatiopn caloric test Nystagmus No nystagmus IX. Glossophangeal Dificulty swallowing Touch pharynx compression of throat region Gag, deglutinatio n, cough No gag no swallowing no cough
  49. 49. X. Vagus Tachycardia? Pressure on eyeball Bradycardia sometime No bradycardia XI. Spinal accessory Few sign seen. Neck muscle weakness.deviation of head to one side Palpation of musculature Muscle tone Lack of muscle tone or atrophy XII.Hypoglossal Earlydisease- tongue deviates towords the unaffected side Late disease- tongue deviates towords the affected side or atrophy and corrugated appearance Observation pull tongue out Retract normaly diviates
  50. 50. Postural reactions  This part of the neurological examination is important in distinguishing neurological disorders from diseases of other body systems.  Proprioceptive placing  This test is designed to evaluate the conscious awareness of limb position and movement in space. It is evaluated by flexing the patient’s paw so that the dorsal surface contacts the floor. It is important to support the patient with an arm under the abdomen if the patient is too weak.
  51. 51.  A normal response is immediate correction to the normal position.  Another test involves putting the patient’s paw on a piece of paper and sliding the paper laterally. A normal patient will reposition its leg when the limb reaches an abnormal position.  Anabnormal reaction is delayed correction of the tested paw. Proprioceptive placing is tested by placing the paw in the abnormal position
  52. 52.  Placing response These are mainly used when proprioceptive positioning or hopping reaction do not confirm a disorder.  Tactile placing- Animal’s eyes are covered and distal part of thoracic limb is place on the edge of the table. When the dorsal surface make contact with the edge, the animal should immediately place it’s foot on the surface.  Visual placing- It is performed by allowing the animal to see the table. Normal animal will reach for surface before the paw touches the table.
  53. 53. Tactile placing
  54. 54.  Hopping reaction-  Hold the animal to support all it’s weight on one limb and move the animal forward or laterally.  Each limb is tested individually and responses on left and right are compared.  Normal animals will hop on the limb while keeping the foot under their body for support.  This is a sensitive test for subtle weakness and asymmetry.
  55. 55. The hopping testing of the right thoracic limb.
  56. 56.  Hemi-walking Hold up the animal on one side of the body and move the patient laterally. Normal reaction is as described for hopping reaction. Hemi-walking
  57. 57.  Wheelbarrowing- Support the animal under the abdomen so that the pelvic limbs are in the air and move the patient forward. Normal animal will move with symmetrical alternate movement of the thoracic limbs.  This test highlights subtle thoracic limb weakness and ataxia. Wheelbarrowing
  58. 58. Spinal reflexes  Spinal reflexes evaluation needs to be done in conjunction with assessment of gait and postural reactions.  The spinal cord segmental in small animals can be divided into four regions.  1. Cranial cervical (C1-C5)  2. Cervicothoracic (C6-T2)  3. Thoracolumbar (T3-L3)  4. Lumbosacral (L4-S3)
  59. 59.  If the lesion that causes spastic tetraparesis is localised in the C1-C5 region then the spinal reflexes usually will be increased or intact.  The lesions of C6-T2 that causes tetraparesis will usually produce increased or intact reflexes in pelvic limbs but decreased or absent in thoracic limbs.  T3-L3 lesions that cause spastic paraparesis will usually cause increased or intact reflexes in pelvic limbs.  The lesion of L4-S3 that cause paraparesis will usually cause decreased to absent spinal reflexes of pelvic limbs.  If the peripheral nervous system is affected then the animals will suffer flaccid tetraparesis
  60. 60.  Withdrawal reflex in the pelvic limbs  This reflex evaluates the integrity of the L4-S2 spinal cord segment and sciatic and femoral nerves. In order to perform this test the digit of the paw needs to be pinched with the fingers. normal response results in the flexion of the hip (femoral nerve), stifle and hock (sciatic nerve).
  61. 61. Withdrawal reflex tested on the right pelvic limb.
  62. 62.  Patellar reflex  This is a monosynaptic reflex that evaluates integrity of the L4-L6 spinal cord segment. The animal needs to be placed in to lateral recumbency with slight stifle flexion. The limb should be held in a neutral position with the examiner’s hand supporting the tested limb. The reflex hammer then hits the patellar tendon and extension of the limb should be observed.
  63. 63. Patellar reflex is tested by hitting the patellar tendon with the reflex hammer
  64. 64.  Withdrawal reflex in the thoracic limbs This reflex evaluates the integrity of the C6-T2 spinal cord segment and brachial plexus and peripheral nerves in the thoracic limb. Pinching of the digits needs to be performed and the flexion of all joints is considered to be a normal response.
  65. 65.  Perineal reflex  This reflex is often overlooked and an important part of the neurological examination. Stimulation of the perineum with the haemostat should result in the contraction of the anal sphincter and flexion of the tail. This reflex tests the integrity of the S1-Cd5 spinal cord segment and the pudendal nerve.
  66. 66. Perineal reflex
  67. 67.  Urinary bladder palpation  Flaccid urinary bladder that is easily expressed is called lower motor neuron bladder and suggests an S1-S3 spinal cord segment lesion, whereas the full and turgid urinary bladder that is not easy to express and has overflow leakage of the urine indicates an upper motor neuron disorder. The abnormal function of the urinary bladder can as well be the result of dysfunction of the autonomic nervous system.
  68. 68. Sensory evaluation  Assessment of the pain sensation requires a noxious stimulus and appropriate response of the animal.
  69. 69.  Nociception testing  It is an important test to do in the cases of spinal cord diseases because it reflects the severity of damage to the spinal cord. The noxious impulse (squeeze of the toe with the fingers or haemostat) is applied to the tested area and the animal must show a behavioural response (turning the head, trying to bite, vocalisation) to say that the nociception is intact.
  70. 70.  Cutaneous trunci reflex (panniculus)  This reflex is performed by pinching the skin of the dorso-lateral aspect of the body between T2 and L4-L5.  A normal reaction to the pinch of the skin is a twitch of the skin (bilaterally, but more prominent on the tested side)
  71. 71.  A variety of systemic disease can cause neurological signs. The cerebral cortex and the peripheral nervous system are the parts of nervous system most susceptible to the systemic diseases. However the white matter changes, brain stem signs and cerebellar signs have also been documented secondary to the systemic conditions.
  72. 72. Neurologic manifestation of systemic disease:  CNS: 1.Hypoxia: a. Pulmonary disease b. Cardiac diseas  infarct  hypoxia  hypertension c. Aneasthetic accident d. Vascular  hypertentions  coagulopathies  vasculitis e. Hypoglycemia  insulin producing neoplasia  insulin over dose  sepsis f. Thiamine deficiency 2.Metabolic  Hepato encephalopathy, renal encephalopathy, hypoadrenocortism, hyperadenocortism,hypothyroidism, hyperthyroidism 3.Electrolyte abnormalities:  Hypercalcemia,hypocalcemia, hyperkalemia, hypokalemia, hypernatremia, hyponatremia 4.Neoplasia:  Primary, metastatic, infract, paraneoplastic syndrome
  73. 73.  Peripheral nervous system 1.Hypoxia: aortic thromboembolism,  a. cardiovascular disease, hypoadrenocortism, renal disease, hypothyroidism ,neoplasia, desiminated intravascular coagulopathy, sepsis etc. 2.Metabolic  hypothyroidism, hypoadrenocortism, hyperadrenocortism, hyperthyroidism. 3.Electrolyte abnormalities  hypokalemia 4.Neoplasia  paraneoplastic syndrome
  74. 74. Hypoxia from systemic disease  Hypoxic encephalopathy is result of reduction of cerebral oxygen supply, either from decrease arterial oxygen tension or reduced cerebral blood flow. Hypoxia can occur secondary to an anesthetic accident, hematologic disorders (especially anemia), or cardiovascular and respiratory failure.  Clinical sign : visual loss (most common in cats during anesthetic accidents), cytotoxic edema in white matter  Treatment: establish normal blood flow and oxygenation in brain  Steroids are contraindicated
  75. 75. Hypertension  A rapid and sustained rise in the blood pressure cause the hypertension.  neurological signs are seizures, ataxia, stupor, and blind ness  Often occur in renal failure  Prevention by controlling seizure and neurological complication by controlling blood pressure
  76. 76. Endocrine /metabolic cause  1. hepatic encephalopathy  Cuases: Porto systemic shunt, macrovasculature dysplasia, idiopathic non cirrhotic portal hypertension, or other cause of liver failure.  Neurological sign: inability to learn new things and behavioral changes; head pressing, blindness, mentation changes and seizure, generalized muscular weakness.  Treatment: decrease the production and absorption of toxin produce by bacteria in GIT.  Low protein diet, antibiotic, RL, H2 blocker  Potassium bromide: 40-60mg/kg Po once daily and gabapentin 20-60mg/kg/day divided dose TID for controlling seizure.
  77. 77.  2. Renal encephalopathy  Toxic substance not excreted due to renal failure can cuase encephalopathic sign similar to hepatic encephalopathy.  Increase concentration of parathyroid hormone and subsequent hypercalcemia contribute to renal encephalopathy  Treatment: control PTH (calcitriol), Lower phosphorus level, treat hypertension.
  78. 78. 3. Hypothyroidism  Acute or chronic progressive central vestibular signs may be the sole clinical sign in dogs with hypothyroidism  Myxedema coma is a rare but life threatening manifestation of hypothyroidism  Clinical signs: mentation changes, hypothermia without shivering, nonpitting skin edema, bradycardia and brain edema  Treatment: adequate ventilation  Normal saline i/v, correct hypothermia, levothyroxine 5ug/kg i/v q 12h. Followed by maintenance thyroid supplementation orally.
  79. 79. 4.Hyperthyroidism  Cats with hyperthyroidism show mild CNS signs that can include hyperactivity, change in sleep/wake cycle, aggression or obtundation.
  80. 80. 5.hyperarenocorticism  Direct compression from a pituitary macroadenoma can cause mild to sever neurologic sign.  Clinical sign: inappetence, mild obtundation, placing and disorientation
  81. 81. 6. Hypoglycemia  The brain since it can not synthesing glucose for normal cellular metabolism  100g/day of glucose requirement by brain  Hypoglycemia cause cellular dysfunction, vascular constriction, reduction in oxygen supply  Hypoglycemia secondary to many condition: poor nutrition, insulinoma, liver failure, hypoadrenocorticism, nonislet cell tumor producing insulin like growth factor, sever polycythemia and sepsis.
  82. 82.  Clinical sign: weakness, disorientation, tremors, partial or generalized seizures, blindness, coma.  Treatment: 2-4ml/kg of 50% or 25% glucose I/V Prednisone: to stimulate gluconeogenesis and glycogenolysis together with frequent feeding of high protein, high fat and high complex carbohydrate diet.
  83. 83. 7. Thiamine deficiency  Essential for decarboxylation of pyruvic acid and other alfa- keto acids.  Thiamine deficiency cause poliencephalomalacia, necrosis and heamorrhage in medial vestibular nuclei, caudal colliculi, cerebellar nodulus and the subcortical grey matter.
  84. 84. Electrolyte abnormalities 1. Hypercalcemia:  Seizure 2.Hypocalcemia  Occur due to renal failure, hypoparathyroidism, eclampsia  Low calcium cause increase membrane excitability in both CNS and muscle.  Weakness, tetany, seizure  Treatment 0.5 – 1.5 mg/kg 10% cacium gluconate I/V over 10-20 minutes.
  85. 85. 3.Hypernatremia/Hyponatremia  Hyponatremia cause cerebral edema and life threatning diffuse encephalopathy.  Hypernatremia cause water out of the brain cells result in reduction of brain volume which may cause rupture of cerebral vessels and focal heamorrhage. .
  86. 86. 4. Neoplasia:  Paraneoplastic syndrome such as hypoglycemia induce by an insulin-producing tumor and hyper calcemia secondary to lymphoma, thymoma, apocrine adenocarcinoma directly affect the CNS. 5. Hyperthermia  The canine brain has an intrinsic thermal resistance. The origin or neurological disturbance in dog and cats with hyperthermia usually from secondary changes such as hepatocellular degeneration, disseminate intravascular coagulation, respiratory alkalosis.  Clinical sign: mentation changes, loss of pupillary light reflex and oculocephalic reflex as well as tetraparesis.
  87. 87. Disease causing PNS signs  Hypoxia: aortic thromboembolism, cardiac failure or other causes  Neurologic sign: chronic exercise intolerance, with pelvic limb weakness, pelvic ataxia, paresis or plegia signs due to ischemic myopathy, neuropathy or myelopathy.
  88. 88. Endocrine/metabolic disorders 1.hypothyroidism:deficiency of ATP cause impairment in Na+/k+ pump reducing axonal transport.  Neurological sign: generalized weakness, muscle atrophy, foca sign like laryngeal paralysis, megaesophagus, facial paralysis, lameness etc 2.Hyperthyroidism  In cat cause neuromuscular weakness with ventroflection of the neck ,a plantigrade stance, exercise intolerance. 3.Hyperadrenocorticism  Muscular weakness
  89. 89. 4.Hypoadrenocorticism  Lethargy, weakness, tremors and collapse  Treatment: glucocorticoids 5.Diabetes mellitus  Pelvic limb with plantigrade stance, difficulty jumping, postural reaction deficits, decrease tendon reflex and muscle atrophy 6.Renal failure  Dogs and cats with chronic renal failure may have weakness associated with renal secondary hyperparathyroidism, which cause peripheral neuropathy and myopathy.
  90. 90. Electrolyte abnormalities 1. hyperkalemia  Renal failure  Hyperkalemia alters the muscle cell resting membrane potential resulting in muscular weakness  Ventroflection of neck and generalize weakness 2.paraneoplastic syndrome  Secondry to insulinoma, adenoma, myeloma, thymoma  Thymoma is a common cause of myasthenia gravis in humans and cats and less common in dogs.

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