Clinical approach to hemiplegia

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Clinical Approach to Hemiplegia:

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Clinical approach to hemiplegia

  1. 1. Manish Chandra Prabhakar MGIMS Reference- Harrison's Internal Medicine 18th edition 1
  2. 2. Stroke • Focal seizures (Todd‟s Palsy)  Migraine  Intracranial neoplasm, Cerebral abscess  Head injury  Subdural hematoma  Epidural hematoma  Hyperglycemia , Hypoglycemia  Acute conversion reaction  Focal encephalitis,meningitis  Drug overdose –cocaine, amphetamine  Hypertensive encephalopathy  Metabolic encephalopathy  Cardiac syncope or syncope from other causes  Postcardiac arrest ischemia  Reference- Harrison's Internal Medicine 18th edition 2
  3. 3. Diagnosis Comments Seizures (postictal) Focal deficits likely are caused by seizure-induced neuronal dysfunction (reversible). May occur with simple partial or generalized seizures. Spontaneous resolution occur over hours (may last up to 48 hours) Hypoglycemia Aphasia or hemiplegia may be present. Variable drowsiness or obtundation. Blood glucose usually <45 mg/dl. Resolution of symptoms with IV glucose. Metabolic encephalopathy Etiologies include hyperosmolar hyperglycemia, hyponatremia, and hepatic encephalopathy. May be associated with altered level of consciousness, poor attention, or disorientation (eg, delirium) asterixis. Conversion reaction Diagnosis of exclusion. Conversion disorder is the most common psychiatric diagnosis. Comorbid psychiatric problems are common. Paresis, paralysis, and movement disorders are common. Reactivation of prior deficits Imaging evidence or history of remote stroke is often apparent. Previous deficit may have resolved 3
  4. 4.   History Neurologic examination Reference- Harrison's Internal Medicine 18th edition 4
  5. 5. The time of symptom onset 1. • • 2. If patient is able to provide information family or friends The nature of symptoms • Abruptly: vascular etiology • Risk factors for vascular disease, history of seizures , migraine, insulin use or drug abuse • Accompanying symptoms (severe „thunderclap‟ headache subarachnoid Hemorrhage) Reference- Harrison's Internal Medicine 18th edition 5
  6. 6.   History of the Present Illness Time of symptom onset Evolution of symptoms, recovery Convulsion or loss of consciousness at onset Headache Chest pain at onset Medical History Prior intracerebral hemorrhage, h/o stroke, Recent head trauma h/o myocardial infarction  Surgical History- Recent surgical procedures  Medications- Anticoagulant therapy  Review of Systems- Gastrointestinal or genitourinary Reference- Harrison's Internal Medicine 18th edition bleeding 6
  7. 7. Record: 3. • • • • • Vital signs Blood glucose level of consciousness severity of deficits Presence of bowel or bladder incontinence Reference- Harrison's Internal Medicine 18th edition 7
  8. 8.   Identify signs of lateralized hemispheric or brainstem dysfunction consistent with focal cerebral ischemia. Level of consciousness, the presence of a gaze deviation, aphasia, neglect or hemiparesis Reference- Harrison's Internal Medicine 18th edition 8
  9. 9.     Validated 15-item scale used to assess key components of the standard neurologic examination and measure stroke severity (lyden et al, 1999) It assess level of consciousness, ocular motility, facial and limb strength, sensory function, coordination , language, speech and attention. Scores range from 0 (normal) to 42 (maximal score). It predicts short-term Internal Medicine Reference- Harrison's and long-term neurologic 18th edition 9 outcomes . (Adams et al, 1999)
  10. 10. Category Scale Definition Category Scale Definition 1a. Level of consciousness 0= Alert 1= Not alert, arousable 2= Not alert, obtunded 3= Unresponsive 5a. Left motor arm 1b. Questions 0= Answers both correctly 1= Answer once correctly 2= Answer neither correctly 0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 5b. Right motor leg 0= No drift 1= Drift before 10 seconds 2= Falls before 10 seconds 3= No effort against gravity 4= No movement 6a. Left motor leg 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 6b. Right motor leg 0= No drift 1= Drift before 5 seconds 2= Falls before 5 seconds 3= No effort against gravity 4= No movement 1c. Commands 0= Performs both tasks correctly 1= Performs one task correctly 2= Performs neither task 2. Gaze 0= Normal 1= Partial gaze palsy 2= Total gaze palsy 3. Visual fields 0= No visual loss 1= Partial hemianopsia 2= Complete hemianopsia 3= Bilateral hemianopsia 4. Facial palsy 0= Normal 7. Ataxia 1= Minor paralysis Reference- Harrison's Internal Medicine 2= Partial paralysis 18th edition 3= Complete paralysis 0= Absent 1= One limib 2= Two limbs
  11. 11. Category Scale Definition 8. Sensory 0= Normal 1= Mild loss 2= Severe loss 9. Language 0= Normal 1= Mild aphasia 2= Severe aphasia 3= Mute or global aphasia 10. Dysarthria 0= Normal 1= Mild 2= Severe 11. Extinction/inatten tion 0= Normal 1= Mild 2= Severe Reference- Harrison's Internal Medicine 18th edition
  12. 12.          Cardio-vascular system Carotid bruit Cardiac murmur Irregularly irregular heart rhythm Unequal extremity pulses Other – Signs of head or neck trauma (occult cervical spine injury) Rales on chest examination (Pneumonia) Bilateral asterixis (metabolic encephalopathy). Reference- Harrison's Internal Medicine 18th edition 12
  13. 13.  “a neurological deficit of sudden onset accompanied by focal dysfunction and symptoms lasting more than 24 hours that are presumed to be of a non-traumatic vascular origin” Reference- Harrison's Internal Medicine 18th edition 13
  14. 14.    Transient Ischemic Attack Stroke in evolution RIND ( Reversible Ischemic Neurological Deficit) Reference- Harrison's Internal Medicine 18th edition 14
  15. 15.  Brief episodes of focal neurological deficits lasting 2-3 minutes to at most a few hours but no longer than 24 hours leaving no residual deficits with complete functional recovery. Reference- Harrison's Internal Medicine 18th edition 15
  16. 16.  a focal brain ischemia in which the deficit improves over a maximum of 72 hours deficits may not completely resolve in all cases Reference- Harrison's Internal Medicine 18th edition 16
  17. 17.  An unusual condition in which a restricted neurological deficit spreads relentlessly over a small period of time, usually hours, to involve adjacent functional areas supplied by the affected artery. Reference- Harrison's Internal Medicine 18th edition 17
  18. 18.              Hypertension ( Systolic or diastolic) Smoking Atrial Fibrillation Myocardial Infarction Hyperlipidemia Diabetes Congestive Heart Failure Acute Alcohol abuse TIA >70% occlusion of the carotid arteries Oral contraceptives in women Hypercoagulopathy Polycythemia and Hemoglobinopathy Age, Gender(Male : Female 3:2), Race, Prior Stroke, and Heredity Reference- Harrison's Internal Medicine 18th edition 18
  19. 19.    3-4% of strokes occur in people aged 15-45 Sickle Cell anemia, tuberculosis Hypercoaguable states   Pregnancy, OCP use, antiphospholipid antibodies, protein C and S deficiencies,nephrotic syndrome Drugs  Cocaine, amphetamines Reference- Harrison's Internal Medicine 18th edition 19
  20. 20.   Ischemic (85% of stroke, Embolic or Thrombosis) Hemorrhagic (15% of stroke) Reference- Harrison's Internal Medicine 18th edition 20
  21. 21. Acute Stroke Ischemic (85%) Hemorrhagic (15%) Subarachnoid H. Thrombotic (55%) Intracerebral & Cerebellar H Embolic (30%) Subdural & Extradural Lacunar (20%) Large vessel (35%) H. and Hematoma Artery-artery embolism Cardioembolic AF, IHD, VHD, Reference- Harrison's Internal Medicine 18th edition 21
  22. 22.    Usually develops at night during sleep Symptoms perceived in morning Suspect in h/o hypercoaguable states, atherosclerosis and collagen vascular disorders Reference- Harrison's Internal Medicine 18th edition 22
  23. 23.     Occurs at any time Frequently during periods of vigorous activity Hx of Atrial fibrillation, valvular vegetations, thromboembolism from MI, ulcerated plaques in carotid system Seizures in 20% of cases
  24. 24. Reference- Harrison's Internal Medicine 18th edition 24
  25. 25. Reference- Harrison's Internal Medicine 18th edition 25
  26. 26.     Occur during stress or exertion Focal deficits rapidly evolve Signs of raised ICT Confusion, coma or immediate death Reference- Harrison's Internal Medicine 18th edition 26
  27. 27. Loss of Consciousness Headache Vomiting Previous TIA Gradual Onset Relation with activity BP Ischemic -ve Hemorrhagic +ve -ve -ve +ve +ve +ve +ve -ve -ve (Sudden and maximal) +ve -ve -ve/mild Reference- Harrison's Internal Medicine 18th edition Moderate/ Severe 27
  28. 28. . Reference- Harrison's Internal Medicine 18th edition 28
  29. 29.      Left (Dominant) Hemisphere Stroke: Common Pattern Aphasia , Difficulty reading, writing, or calculating Majority of right handed and most left handed patients have dominance for speech and language located in the left hemisphere Left hemisphere infarction is characterized by aphasia (both motor [Broca‟s] and sensory [Wernicke‟s]) and apraxia Right Hemiparesis Right-sided sensory loss Right visual field defect ReferencePoor right conjugateHarrison's Internal Medicine gaze 18th edition 29
  30. 30. Right (Non-dominant) Hemisphere Stroke: Common Pattern  Less predictable syndromes Left Hemiparesis Left-sided sensory loss       Poor left conjugate gaze Dysarthria Attention defects: extinction and neglect Spatial disorientation Behavioral changes: acute confusion and delirium Defect of left visual field Reference- Harrison's Internal Medicine 18th edition 30
  31. 31. Reference- Harrison's Internal Medicine 18th edition 31
  32. 32. Reference- Harrison's Internal Medicine 18th edition 32
  33. 33. Reference- Harrison's Internal Medicine 18th edition 33
  34. 34. Stroke Syndromes Large-vessel stroke within anterior ciculation Internal carotid artery and Its branches ACA MCA Large-vessel stroke within posterior ciculation PCA Small-vessel disease of either vascular bed Basilar Artery Vertebral and posterior inferior cerebellar Reference- Harrison's Internal Medicine arteries 18th edition 34
  35. 35. . Reference- Harrison's Internal Medicine 18th edition 35
  36. 36. Anterior Circulation  From carotid system  Supplies 80% of brain Posterior Circulation  From vertebral system  Supplies 20% of brain Reference- Harrison's Internal Medicine 18th edition 36
  37. 37.  CA arises from the innominate artery on the right and aortic arch on the left. At level of upper neck CA branches into internal and external  the internal carotid artery terminates into the middle (MCA) and anterior (ACA) cerebral arteries Reference- Harrison's Internal Medicine 18th edition 37
  38. 38. Reference- Harrison's Internal Medicine 18th edition 38
  39. 39. Reference- Harrison's Internal Medicine 18th edition 39
  40. 40.  o o   The ACA is divided into two segments: the precommunal (A1) which connects the internal carotid artery to the anterior communicating artery the postcommunal (A2) segment - distal to the anterior communicating artery . The A1 segment gives rise to several deep penetrating branches that supply the anterior limb of the internal capsule, the anterior perforate substance, amygdala, anterior hypothalamus, and the inferior part of the head of the caudate nucleus. A2 segment - Supplies basal and medial aspects of the cerebral hemispheres, extends to anterior two Reference- Harrison's Internal thirds of parietal lobe. edition Medicine 18th 40
  41. 41. Reference- Harrison's Internal Medicine 18th edition 41
  42. 42. Reference- Harrison's Internal Medicine 18th edition 42
  43. 43. SIGNS AND SYMPTOMS STRUCTURES INVOLVED  Paralysis of opposite foot and leg   A lesser degree of paresis of opposite arm  Cortical sensory loss over toes, foot, and leg a Urinary incontinence      Contralateral grasp reflex, sucking reflex    Abulia (akinetic mutism), slowness, intermittent interruption, lack of spontaneity, whispering, distraction to sights and sounds  Impairment of gait and stance (gait apraxia)  Dyspraxia of left limbs   Motor leg area Arm area of cortex or fibers descending to corona radiata Sensory area for foot and leg Sensorimotor area in paracentral lobule Medial surface of the posterior frontal lobe; likely supplemental motor area probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes Frontal cortex near leg motor area Reference- Harrison's Internal Medicine 18th edition 43
  44. 44.  MCA supply the lateral surface of the hemisphere except for (1) frontal pole and a strip along the superomedial border of the frontal and parietal lobes supplied by the ACA (2) lower temporal and occipital pole convolutions supplied by PCA  The proximal MCA (M1 segment) gives rise to penetrating branches (lenticulostriate arteries) - supply Reference- Harrison's Internal Medicine 18th edition the putamen, outer globus pallidus, posterior limb of the 44
  45. 45.  In the sylvian fissure, the MCA divides into superior and inferior divisions (M2 branches)  Branches from the superior division supply the frontal and superior parietal cortex and those of the inferior division Supply the inferior parietal and temporal cortex Reference- Harrison's Internal Medicine 18th edition 45
  46. 46. Reference- Harrison's Internal Medicine 18th edition 46
  47. 47.      If the entire MCA is occluded at its origin contralateral hemiplegia, hemianesthesia, homonymous hemianopia, and gaze preference to the ipsilateral side. Dysarthria is common because of facial weakness. When the dominant hemisphere is involved, global aphasia is present when the nondominant hemisphere is affected, anosognosia, constructional apraxia, and neglect are found . Reference- Harrison's Internal Medicine 18th edition 47
  48. 48.     Partial syndromes due to embolic occlusion of a single branch include hand, or arm and hand, weakness alone or facial weakness with Broca aphasia, with or without arm weakness A combination of sensory disturbance, motor weakness, and Broca‟s aphasia suggests that an embolus has occluded the proximal superior division and infarcted large portions of the frontal and parietal cortices . Wernicke's aphasia without weakness – involvement of the inferior division of the MCA supplying the posterior part (temporal cortex) of the dominant hemisphere Hemineglect or spatial agnosia without weakness Reference- Harrison's inferior indicates – involvement ofInternal Medicine division of the 18th edition 48
  49. 49.     Signs and symptoms: Structures involved Paralysis of the contralateral face, arm, and leg; sensory impairment over the same area : Somatic motor area for face and arm and the fibers descending from the leg area to enter the corona radiata and corresponding somatic sensory system Motor aphasia: dominant hemisphere Motor speech area of the aphasia, word deafness, anomia, jargon speech, sensory agraphia, acalculia, alexia, finger agnosia, right-left confusion (the last four comprise the Gerstmann syndrome): Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere Reference- Harrison's Internal Medicine 18th edition 49
  50. 50.  Anosognosia , unilateral neglect, agnosia for the left half of external space, dressing "apraxia," constructional "apraxia," distortion of visual coordinates, inaccurate localization in the half field, impaired ability to judge distance, upside-down reading, visual illusions: Nondominant parietal lobe Optic radiation deep to second temporal convolution  Homonymous hemianopia:  Paralysis of conjugate gaze to the opposite Reference- Harrison's Internal Medicine 18th edition 50
  51. 51.  This artery arises from the internal carotid artery and supplies the posterior limb of the internal capsule and the white matter posterolateral to it  The complete syndrome of anterior choroidal artery occlusion consists of contralateral hemiplegia, hemianesthesia and homonymous hemianopia.  Since this territory is also supplied by penetrating vessels of the proximal MCA and the posterior communicating and posterior choroidal arteries, minimal deficits may occur, and patients frequently recover substantially. Reference- Harrison's Internal Medicine 18th edition 51
  52. 52.    With a competent circle of Willis, occlusion may go unnoticed. If the thrombus propagates up the internal carotid artery into the MCA or embolizes it, symptoms are identical to proximal MCA occlusion. When the origins of both the ACA and MCA are occluded at the top of the carotid artery, abulia or stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosognosia. Reference- Harrison's Internal Medicine 18th edition 52
  53. 53.   In addition to supplying the ipsilateral brain, the internal carotid artery perfuses the optic nerve and retina via the ophthalmic artery. In 25% of symptomatic internal carotid disease, recurrent transient monocular blindness (amaurosis fugax) warns of the lesion. Reference- Harrison's Internal Medicine 18th edition 53
  54. 54. 2 Vertebral arteries basilar artery posterior cerebral arteries  Reference- Harrison's Internal Medicine 18th edition 54
  55. 55.  In 75% of cases, both PCAs arise from bifurcation of basilar artery; in 20%, one has its origin from ipsilateral internal carotid artery; in 5%, both originate from respective ipsilateral ICA Two clinical syndromes are commonly observed with occlusion of the PCA: (1) P1 syndrome: midbrain, subthalamic, and thalamic signs, due to disease of the Proximal P1 segment of the PCA or its penetrating branches (thalamogeniculate, posterior choroidal )  (2) P2 syndrome: cortical temporal & occipital lobe signs, due to occlusion of the P2 segment distal to the junction of the PCA with the posterior communicating artery. Reference- Harrison's Internal Medicine 18th edition 55
  56. 56. Reference- Harrison's Internal Medicine 18th edition 56
  57. 57.    P1 Syndromes Infarction usually occurs in the ipsilateral subthalamus and medial thalamus and in the ipsilateral cerebral peduncle and midbrain. A third nerve palsy with contralateral ataxia (Claude's syndrome) or with contralateral hemiplegia (Weber's syndrome) may result.  ataxia - the red nucleus or dentatorubrothalamic tract  contralateral hemiballismus - subthalamic nucleus    Extensive infarction in the midbrain and subthalamus occurring with bilateral proximal PCA occlusion presents as coma, unreactive pupils, bilateral pyramidal signs, and decerebrate rigidity. Occlusion of the penetrating branches of thalamic and thalamogeniculate arteries produces less extensive thalamic & thalamocapsular lacunar syndromes. The thalamic Déjérine-Roussy syndrome consists of contralateral Reference- Harrison's Internal Medicine hemisensory loss followed later edition agonizing, searing or burning 18th by an 57
  58. 58.         P2 Syndromes Occlusion of the distal PCA causes infarction of the medial temporal and occipital lobes. Contralateral homonymous hemianopia with macula sparing is the usual manifestation. If the visual association areas are spared and only the calcarine cortex is involved, the patient may be aware of visual defects. Medial temporal lobe and hippocampal involvement may cause an acute disturbance in memory, particularly if it occurs in the dominant hemisphere. If the dominant hemisphere is affected and the infarct extends to involve the splenium of the corpus callosum, the patient may demonstrate alexia without agraphia. Visual agnosia for faces, objects, mathematical symbols, and colors and anomia with paraphasic errors may also. Occlusion of the Reference- Harrison's Internal Medicine 18th edition posterior cerebral artery can produce visual 58
  59. 59.     Bilateral infarction in the distal PCAs produces cortical blindness (blindness with preserved pupillary light reaction). The patient is often unaware of the blindness or may even deny it (Anton's syndrome). Patients may experience persistence of a visual image for several minutes despite gazing at another scene (palinopsia) or an inability to synthesize the whole of an image (asimultanagnosia). Embolic occlusion of the top of the basilar artery can produce any or all of the central or peripheral territory symptoms. The hallmark is the sudden onset of bilateral signs, including pupillary asymmetry or lack of Reference- Harrison's Internal Medicine reaction to light 18th edition 59
  60. 60.    The vertebral artery, which arises from the innominate artery on the right and the subclavian artery on the left, consists of four segments. V1 extends from its origin to its entrance into the 6 th transverse vertebral foramen. V2 traverses the vertebral foramina from C6 to C2. V3 passes through the transverse foramen and circles around the arch of the atlas to pierce the dura at the foramen magnum.  V4 segment courses upward to join the other vertebral artery to form the basilar artery; only the fourth segment gives rise to branches that supply the brainstem and cerebellum.  The posterior inferior cerebellar artery (PICA) in its proximal segment supplies the lateral medulla and, in its distal branches, the inferior surface of the cerebellum.  Reference- Harrison's Internal Medicine 18th edition 60
  61. 61.  If the subclavian artery is occluded proximal to the origin of the vertebral artery, there is a reversal in the direction of blood flow in the ipsilateral vertebral artery. Exercise of the ipsilateral arm may increase demand on vertebral flow, producing posterior circulation TIAs, or "subclavian steal.” Reference- Harrison's Internal Medicine 18th edition 61
  62. 62.     Branches of the basilar artery supply the base of the pons and superior cerebellum and fall into three groups: Paramedian , 7–10 in number, which supply a wedge of pons on either side of the midline short circumferential, 5–7 in number, that supply the lateral two-thirds of the pons and middle and superior cerebellar peduncles bilateral long circumferential (superior cerebellar and anterior inferior cerebellar arteries), which course around the pons to supply the cerebellar hemispheres. Reference- Harrison's Internal Medicine 18th edition 62
  63. 63. Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery)  On side of lesion Paralysis with atrophy of one-half half the tongue: Ipsilateral twelfth nerve  On side opposite to lesion Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral pyramidal tract and 63
  64. 64. Lateral medullary syndrome (occlusion of any of the five vessels may be responsible –vertebral, posterior inferior cerebellar, superior, middle or inferior lateral medullary arteries)   On side of lesion Pain, numbness, impaired sensation over one-half the face: Descending tract and nucleus fifth nerve  Ataxia of limbs, falling to side of lesion: restiform body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract  Nystagmus , diplopia , vertigo, nausea, vomiting: Vestibular nucleus  Horner's syndrome ( miosis , ptosis , Reference- Harrison's Internal Medicine decreased sweating): 18th edition 64
  65. 65.    Dysphagia, hoarseness, p aralysis of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and tenth nerves Loss of taste: Nucleus and tractus solitarius Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei    Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus On side opposite to lesion Impaired pain and thermal sense over half the body, sometimes Harrison's Internal Medicine Reference18th edition face: Spinothalamic 65
  66. 66.    Total Unilateral medullary syndrome (occlusion of vertebral artery)  Combination of medial and lateral syndromes Lateral pontomedullary syndrome (occlusion of vertebral artery)  Combination of lateral medullary and lateral inferior pontine syndrome Basilar artery syndrome  Combination of brainstem syndromes plus those arising in PCA distribution Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities): Bilateral long tract; cerebellar and peripheral cranial nerves Paralysis or weakness of all extremities, plus all Reference- Harrison's Internal Medicine 18th edition bulbar musculature: Corticobulbar and corticospinal 66
  67. 67. Medial Superior pontine syndrome (paramedian branches of upper basilar artery)  On side of lesion Cerebellar ataxia (probably):  Internuclear ophthalmoplegia:   Superior and/or middle cerebellar peduncle Medial longitudinal fasciculus Myoclonic syndrome, palate, pharynx, vocal cords, respiratory apparatus, face, oculomotor apparatus, etc.: central tegmental bundle, dentate projection, inferior olivary nucleus    On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract Rarely touch, vibration, and position are affected: Medial lemniscus 67
  68. 68. Lateral superior pontine syndrome (Syndrome of superior cerebellar artery)  On side of lesion  Ataxia of limbs and gait, falling to side of lesion: Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus  Dizziness, nausea, vomiting; horizontal nystagmus: Vestibular nucleus  Paresis of conjugate gaze (ipsilateral): Pontine contralateral Reference- Harrison's Internal Medicine gaze 18th edition 68
  69. 69.     Miosis, ptosis, decreased sweating over face (Horner's syndrome): Descending sympathetic fibers Tremor:Dentate nucleus, superior cerebellar peduncle On side opposite lesion Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic tract  Impaired touch, vibration, and position sense : Medial Reference- Harrison's Internal Medicine lemniscus (lateral 18th edition 69
  70. 70. Medial midpontine syndrome (paramedian branch of midbasilar artery)  On side of lesion  Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine nuclei   On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract  Variable impaired touch and proprioception when lesion extends 70
  71. 71. Lateral midpontine syndrome (Short circumferential artery)    On side of lesion Ataxia of limbs: Middle cerebellar peduncle Paralysis of muscles of mastication: Motor fibers or nucleus of fifth nerve  Impaired sensation over side of face: Sensory fibers or nucleus of fifth nerve   On side opposite lesion Impaired pain and thermal sense on limbs 71
  72. 72. Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)   On side of lesion Paralysis of conjugate gaze to side of lesion (preservation of convergence): Center for  conjugate lateral gaze Nystagmus: Vestibular nucleus  Ataxia of limbs and gait: Likely  Diplopia on lateral gaze:    middle cerebellar peduncle Abducens nerve On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower pons Impaired tactile and proprioceptive sense over half of the body: Medial lemniscus 72
  73. 73. Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery)   On side of lesion Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia: Vestibular nerve or nucleus        Facial paralysis: Seventh nerve Paralysis of conjugate gaze to side of lesion: Center for conjugate lateral gaze Deafness, tinnitus: Auditory nerve or cochlear nucleus Ataxia: Middle cerebellar peduncle and cerebellar hemisphere Impaired sensation over face: Descending tract and nucleus fifth nerve On side opposite lesion Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract Reference- Harrison's Internal Medicine 18th edition 73
  74. 74. Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries)   On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers   On side opposite lesion Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus Reference- Harrison's Internal Medicine cerebri 18th edition 74
  75. 75. Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)   On side of lesion Eye "down and out" secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers and/or third nerve nucleus   On side opposite lesion Hemiataxia , hyperkinesias, tremor: Internal Medicine Reference- Harrison's Red nucleus, 18th edition 75
  76. 76. Brain Stem Stroke: Common Pattern            Hemiparesis or tetraparesis Sensory loss Diplopia Facial numbness Facial weakness (lower motor neurone) Nystagmus, vertigo Dysphagia, Dysarthria Ataxia, hiccups, vomiting Horner's syndrome Altered consciousness Crossed signs Reference- Harrison's Internal Medicine 18th edition 76
  77. 77.  Small penetrating branches  HT, DM, Atherosclerosis  Pure motor hemiplegia – Lenticulostriate territory  Pure sensory stroke – Lat. Thalamus  Clumsy hand dysarthria  ataxic hemiparesis – ataxia Reference- Harrison's Internal Medicine 18th edition 77
  78. 78. Reference- Harrison's Internal Medicine 18th edition 78
  79. 79.     occurs in vulnerable areas supplied by distal distribution cerebral arteries during periods of hypotension infarction between the anterior and middle cerebral arteries presents with hemiparesis and hemianesthesia, predominantly in the leg dominant hemisphere infarctions: decrease in verbal ability with preserved comprehension Infarction involving the posterior watershed area presents with homonymous hemianopia +/Reference- Harrison's Internal Medicine hypoesthesia in the face and legs 18th edition 79

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