Introduction to neurosciences to 4 th year medical students
Upcoming SlideShare
Loading in...5
×
 

Introduction to neurosciences to 4 th year medical students

on

  • 635 views

A presentation introducing medical students who have just finished their basic sciences years to clinical neurosciences.

A presentation introducing medical students who have just finished their basic sciences years to clinical neurosciences.

Statistics

Views

Total Views
635
Views on SlideShare
475
Embed Views
160

Actions

Likes
0
Downloads
6
Comments
0

8 Embeds 160

http://walidmaani.blogspot.com 151
http://www.walidmaani.blogspot.com 3
http://walidmaani.blogspot.com.es 1
http://walidmaani.blogspot.de 1
http://walidmaani.blogspot.mx 1
http://walidmaani.blogspot.ae 1
http://walidmaani.blogspot.ru 1
http://walidmaani.blogspot.it 1
More...

Accessibility

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

Introduction to neurosciences to 4 th year medical students Introduction to neurosciences to 4 th year medical students Presentation Transcript

  • AN INTRODUCTION TO CLINICAL NEUROSIENCES WALID MAANI PROFESSOR OF NEUROSURGERY08/18/12 FOURTH YEAR LECTURE 1
  • IT IS VERY DIFFICULT TO DO THIS IN ONE HOUR08/18/12 FOURTH YEAR LECTURE 2
  • PRESENTATON OF CENTRAL NERVOUSSYSTEM PROBLEMS• HOW DO CRANIAL LESIONS PRESENT?• HOW DO SPINAL PROBLEMS PRESENT?08/18/12 FOURTH YEAR LECTURE 3
  • PRESENTATION OF CRANIAL LESIONS SULCI THIS IS HOW THE INTRACRANIAL CONTENTS ARE VENTRICLE ARRANGED AS SEEN ON MAGNETIC CHOROID PLEXUS RESONANCE MIDLINE IMAGING (MRI) T1 WEIGHTED MRI08/18/12 FOURTH YEAR LECTURE 4
  • PRESENTATION OF CRANIAL LESIONS SUDDEN:  CEREBRO-VASCULAR ACCIDENTS  INTRACEREBRAL HEMORRHAGE  SUBARACHNOID HEMORRHAGE  INFARCTION  TRAUMA RAPID:  INFECTION GRADUAL:  NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 5
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION TRAUMA RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 6
  • INTRACEREBRAL HEMORRHAGE08/18/12 FOURTH YEAR LECTURE 7
  • INTRACEREBRAL HEMORRHAGE MAY CAUSE DEATH MAY CAUSE LOC DESTRUCTION OF BRAIN AREAPRESENTS WITH: SUDDEN HEADACHE SUDDEN PARALYSIS SPEECH PROBLEMS SENSORY DISTURBANCES VISUAL DISTURBANCES08/18/12 FOURTH YEAR LECTURE 8
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION TRAUMA RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 9
  • SUBARACHNOID HEMORRHAGE08/18/12 FOURTH YEAR LECTURE 10
  • SUBARACHNOID HEMORRHAGE MAY CAUSE DEATH SUDDEN HEADACHE LOC EPILEPSY NECK RIGIDITY MAY BE ASSOCITAED WITH PARALYSIS IF ACCOMPANIED BY INTRACEREBRAL HEMORRHAGE08/18/12 FOURTH YEAR LECTURE 11
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION TRAUMA RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 12
  • INFARCTION08/18/12 FOURTH YEAR LECTURE 13
  • INFARCTION MAY BE ISCHAEMIC MAY BE HEMORRHAGIC MAY BE UN-NOTICED LOC EPILEPSY DESTRUCTION OF BRAIN:  PARALYSIS  SPEECH PROBLEMS  VISUAL PROBLEMS  SENSORY PROBLEMS08/18/12 FOURTH YEAR LECTURE 14
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION TRAUMA RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 15
  • TRAUMAEXTRADURAL HEMATOMA BRAIN CONTUSION 08/18/12 FOURTH YEAR LECTURE 16
  • TRAUMA HISTORY OF TRAUMA DEATH LOC EPILEPSY PARALYSIS SPEECH PROBLEMS VISUAL PROBLEMS08/18/12 FOURTH YEAR LECTURE 17
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 18
  • INFECTIONTHE UNDERSURFACE OF THE BRAIN IN MENINGITIS 08/18/12 FOURTH YEAR LECTURE 19
  • INFECTION GRADUAL FEVER LETHARGY NECK RIGIDITY LOC EPILEPSY PARALYSIS DEATH08/18/12 FOURTH YEAR LECTURE 20
  • PRESENTATION OF CRANIAL LESIONS SUDDEN: CEREBRO-VASCULAR ACCIDENTS INTRACEREBRAL HEMORRHAGE SUBARACHNOID HEMORRHAGE INFARCTION RAPID: INFECTION GRADUAL NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 21
  • NEOPLASTIC LESIONSBRAIN METASTASES BRAIN GLIOMA08/18/12 FOURTH YEAR LECTURE 22
  • NEOPLASTIC LESIONS GRADUAL EPILEPSY PARALYSIS SENSORY PROBLEMS SPEECH PROBLEMS VISUAL PROBLEMS BALANCE PROBLEMS BEHAVIOUR CHANGES08/18/12 FOURTH YEAR LECTURE 23
  • THE NORMAL PICTURET1 WEIGHTED MRI T2 WEIGHTED MRI08/18/12 FOURTH YEAR LECTURE 24
  • NOW IMAGINE IF WE ADD SOMETHING ELSE TO THE CONTENTSDISPLACED BRAIN OEDEMA MIDLINE BRAIN OEDEMATHE ORIGINAL DEFORMED MIDLINE VENTRICLE TUMOR MASS TUMORS MENINGIOMA ON MRI T2 MULTIPLE LESIONS ON CT 08/18/12 FOURTH YEAR LECTURE 25
  • ADDITION OF NEW CONTENTS• INCREASE IN THE INTRACRANIAL PRESSURE• IRRITATION OF THE AREA• PRESSURE ON THE AFFECTED AREA• DESTRUCTION OF THE AFFECTED AREA• OBSTRUCTION OF THE CSF PATHWAYS• HORMONAL PROBLEMS 08/18/12 FOURTH YEAR LECTURE 26
  • INCREASE IN THE INTRACRANIAL PRESSURE• SYMPTOMS: • HEADACHE • VOMITING • VISUAL PROBLEMS • INCREASE IN THE SIZE OF THE HEAD08/18/12 FOURTH YEAR LECTURE 27
  • INCREASE IN THE INTRACRANIAL PRESSURE• SYMPTOMS: IS A MORNING • HEADACHE HEADACHE WHICH • VOMITING RESPONDS TO • VISUAL PROBLEMS SIMPLE ANALGESIA. IT • INCREASE IN THE SIZE DOES NOT INDICATE OF THE HEAD TYPE OF PROBLEM08/18/12 FOURTH YEAR LECTURE 28
  • INCREASE IN THE INTRACRANIAL PRESSURE IS A MORNING• SYMPTOMS: VOMITING AND IS • HEADACHE PROJECTILE IN • VOMITING NATURE. IT RESEMBLES • VISUAL PROBLEMS • MIGRAINE VOMITING INCREASE IN THE SIZE OF THE HEAD OR THE VOMITING ASSOCIATED WITH PREGNANCY08/18/12 FOURTH YEAR LECTURE 29
  • INCREASE IN THE INTRACRANIAL PRESSURE COULD BE IN THE• SYMPTOMS: FORM OF BLURRED • HEADACHE VISION OR DECREASED • VOMITING ACUITY OR FIELD • VISUAL PROBLEMS • DEFECT IN ONE OR INCREASE IN THE SIZE OF THE HEAD BOTH EYES. DEFECTS CAN INDICATE SITE OF PATHOLOGY08/18/12 FOURTH YEAR LECTURE 30
  • INCREASE IN THE INTRACRANIAL PRESSURE• SYMPTOMS: THIS OCCURS • HEADACHE ONLY IN CHILDREN • VOMITING BECAUSE THE • INCREASE IN THE SIZE OF THE HEAD CRANIAL SUTURES HAVE NOT UNITED YET.08/18/12 FOURTH YEAR LECTURE 31
  • INCREASE IN THE INTRACRANIAL PRESSURE IS SWELLING OF THE• SIGNS OPTIC DISC AND • PAPILLOEDEMA IS SEEN BY OPHTHALMOSCOPY NORMAL FUNDUS08/18/12 PAPILLOEDEMA LECTURE FOURTH YEAR 32
  • IRRITATION OF THE AREA THERE ARE MANY FORMS THIS LEADS TO OF EPILEPSY: EPILEPSY IF THE GRAND MAL LESION IS ON THE PETIT MAL PARTIAL COMPLEX SURFACE OF THE ETC.CEREBRUM. THE CORTEX EPILEPSY MAY LEAD TO:MUST BE IRRITATED TO SUFFOCATION PRODUCE EPILEPSY TEMPORARY PARALYSIS (TODD’S) OR PERMANENT BRAIN DAMAGE08/18/12 FOURTH YEAR LECTURE 33
  • PRESSURE ON THE AFFECTED AREA or tum val e of o• DEPENDS ON WHETHER: Sit r rem a fte • SUPRATENTORIAL • INFRATENTORIAL 08/18/12 FOURTH YEAR LECTURE 34
  • PRESSURE ON THE AFFECTED AREADESTRUCTION OF THE AFFECTED AREA• SUPRATENTORIAL: • FRONTAL • TEMPORAL • PARIETAL • OCCIPITAL• INFRATENTORIAL: • LATERAL • MIDLINE08/18/12 FOURTH YEAR LECTURE 35
  • PRESSURE ON THE AFFECTED AREADESTRUCTION OF THE AFFECTED AREA SUPRA TENTORIAL LESIONS: FRONTAL LOBE AFFECTION: DISTURBANCE OF ORIENTATION BEHAVIORAL CHANGES SPHINCTER PROBLEMS MOTOR SYMPTOMS ON THE OPPOSITE SIDE08/18/12 FOURTH YEAR LECTURE 36
  • PRESSURE ON THE AFFECTED AREADESTRUCTION OF THE AFFECTED AREA TEMPORAL LOBE AFFECTION: EXPRESSIVE DYSPHASIA OR APHASIA VISUAL FIELD DEFECTS SENSORY SYMPTOMS ON THE OPPOSITE SIDE MOTOR SYMPTOMS ON THE OPPOSITE SIDE08/18/12 FOURTH YEAR LECTURE 37
  • PRESSURE ON THE AFFECTED AREADESTRUCTION OF THE AFFECTED AREA PARIETAL LOBE AFFECTION:  RECEPTIVE DYSPHASIA OR APHASIA  SENSORY SYMPTOMS ON THE OPPOSITE SIDE  MOTOR SYMPTOMS ON THE OPPOSITE SIDE  ASTEREOGNOSIS  LACK OF TWO POINT DISCRIMINATION  SPATIAL DISORIENTATION  FINGER AGNOSIA08/18/12 FOURTH YEAR LECTURE 38
  • PRESSURE ON THE AFFECTED AREADESTRUCTION OF THE AFFECTED AREA OCCIPITAL LOBE AFFECTION:  VISUAL FIELD DEFECTS (HOMONYMOUS HEMIANOPIA)08/18/12 FOURTH YEAR LECTURE 39
  • PRESSURE ON THE AFFECTED AREA DESTRUCTION OF THE AFFECTED AREA INFRATENTORIAL TUMORS  ATAXIA  NYSTAGMUS  OBSTRUCTION OF CSF FLOWTOP:MEDULLOBLASTOABOTTOM:ASTROCYTOMA 08/18/12 FOURTH YEAR LECTURE 40
  • DESTRUCTION COULD RESULT FROMOCCLUSION OF A MAJOR ARTERY INTERNAL CAROTID ARTERY ANTERIOR CEREBRAL MIDDLE CEREBRAL BASILAR ARTERY POSTERIOR CEREBRAL08/18/12 FOURTH YEAR LECTURE 41
  • DESTRUCTION COULD RESULT FROM OCCLUSIONOF A MAJOR ARTERY  INTERNAL CAROTID ARTERY ANTERIOR CEREBRAL MIDDLE CEREBRAL  BASILAR ARTERY POSTERIOR CEREBRAL 08/18/12 FOURTH YEAR LECTURE 42
  • DESTRUCTION COULD RESULT FROM OCCLUSION OF A MAJOR ARTERY • CONTRALATERAL INTERNAL CAROTID HEMIPLEGIA ARTERY • MILD SENSORY DEFICIT  ANTERIOR CEREBRAL  MIDDLE CEREBRAL • MENTAL CONFUSION BASILAR ARTERY • CLOUDING OF THE  POSTERIOR CEREBRAL CONSCIOUSNESS 08/18/12 FOURTH YEAR LECTURE 43
  • DESTRUCTION COULD RESULT FROM OCCLUSION OF A MAJOR ARTERY INTERNAL CAROTID • COMA  ARTERY • CONTRALATERAL  ANTERIOR CEREBRAL FLACCID HEMIPLEGIA  MIDDLE CEREBRAL • HEMIANESTHESIA BASILAR ARTERY • HEMIANOPIA  POSTERIOR CEREBRAL • MOTOR APHASIA • SENSORY APHASIA 08/18/12 FOURTH YEAR LECTURE 44
  • DESTRUCTION COULD RESULT FROM OCCLUSION OF A MAJOR ARTERY INTERNAL CAROTID ARTERY  ANTERIOR CEREBRAL • CONTRALATERAL  MIDDLE CEREBRAL HEMIANESTHESIA BASILAR ARTERY • CONTRALATERAL  POSTERIOR CEREBRAL HOMONYMOUS HEMIANOPIA • SENSORY APHASIA 08/18/12 FOURTH YEAR LECTURE 45
  • OBSTRUCTION OF CSF PATHWAYS WILL LEAD TO DILATATION OF THE VENTRICULAR SYSTEM AND SIGNS AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE. SEEPAGE OF CSF DILATED VENTRICLES NORMAL ABNORMAL08/18/12 FOURTH YEAR LECTURE 46
  • OBSTRUCTION OF CSF PATHWAYS IN INFANTS AND LITTLE CHILDERN IT WILL LEAD TO ENLARGMENT OF THE HEAD DUE TO THE FACT THAT SUTURES ARE NOT CLOSED. HYDROCEPHALUS COULD BE OBSTRUCTIVE OR COMMUNICATING08/18/12 FOURTH YEAR LECTURE 47
  • OBSTRUCTION OF CSF PATHWAYS BESIDE ENLARGMENT OF THE HEAD, DILATATION OF THE VENTRICULAR SYSTEM WILL LEAD TO DETERIORATION OF THE LEVEL OF CONSCIOUSNESS.ASSESSMENT OF THE LOC IS DONE GENERALLY BY THE USE OF THE GLASGOW COMA SCALE (GCS)08/18/12 FOURTH YEAR LECTURE 48
  • OBSTRUCTION OF CSF PATHWAYS THE GLASGOW COMA SCALE Points Eye Opening Best Verbal Response Best Motor Response 6 Follows command 5 Appropriate Localizes pain 4 Inappropriate Withdraws 3 To voice Moaning Flexion 2 To pain Incomprehensible Extension 08/18/12 FOURTH YEAR LECTURE 49
  • THE GLASGOW COMA SCALE• A NORMAL PERSON WOULD SCORE 15 • 6 FROM FOLLOWING COMMAND • 5 FROM APPROPRIATE VERBAL RESPONSE • 4 FROM SPONTANEOUS EYE OPENING• A DEAD PERSON SCORES 3 • 1 FROM NO MOTOR RESPONSE • 1 FROM NO VERBAL REPONSE • 1 FROM NO EYE OPENING08/18/12 FOURTH YEAR LECTURE 50
  • HORMONAL PROBLEMS USUALLY IN PROBLEMS OF THE PITUITARY GLAND OR THE PINEAL BODY. INCREASE PITUITARY SECRETION LEADS TO:  ACROMEGALLY  GIGANTISM  GALACTORRHOEA  AMENORRHOEA DECREASED SECRETION LEADS TO: HYPOPITUITRISM08/18/12 FOURTH YEAR LECTURE 51
  • HORMONAL PROBLEMS USUALLY IN PROBLEMS OF THE PITUITARY GLAND OR THE PINEAL BODY. INCREASE PITUITARY SECRETION LEADS TO:  ACROMEGALLY  GIGANTISM  GALACTORRHOEA  AMENORRHOEA DECREASED SECRETION LEADS TO: HYPOPITUITRISM08/18/12 FOURTH YEAR LECTURE 52
  • HORMONAL PROBLEMS DUE TO THE OVER SECRETION OF THE GROWTH HORMONE AFTER THE EPIPHYSIS HAD UNITED: INCREASE NOSE SIZE INCREASE HAND SIZE INCREASE FEET SIZE INCREASE JAW SIZE08/18/12 FOURTH YEAR LECTURE 53
  • HORMONAL PROBLEMS USUALLY IN PROBLEMS OF THE PITUITARY GLAND OR THE PINEAL BODY. INCREASE PITUITARY SECRETION LEADS TO:  ACROMEGALLY  GIGANTISM  GALACTORRHOEA  AMENORRHOEA DECREASED SECRETION LEADS TO: HYPOPITUITRISM08/18/12 FOURTH YEAR LECTURE 54
  • HORMONAL PROBLEMS DUE TO THE OVER SECRETION OF THE GROWTH HORMONEBEFORE THE EPIPHYSIS HAD UNITED.08/18/12 FOURTH YEAR LECTURE 55
  • HORMONAL PROBLEMS USUALLY IN PROBLEMS OF THE PITUITARY GLAND OR THE PINEAL BODY. INCREASE PITUITARY SECRETION LEADS TO:  ACROMEGALLY  GIGANTISM  GALACTORRHOEA  AMENORRHOEA DECREASED SECRETION LEADS TO: HYPOPITUITRISM08/18/12 FOURTH YEAR LECTURE 56
  • EXAMPLES OF PITUITARY LESIONS08/18/12 FOURTH YEAR LECTURE 57
  • PRESENTATION OF SPINAL LESIONS• SUDDEN: • VASCULAR ACCIDENTS • INTRASPINAL HEMORRHAGE • INFARCTION• RAPID: • INFECTION • DEMYLINATION• GRADUAL: • NEOPLASTIC LESIONS08/18/12 FOURTH YEAR LECTURE 58
  • PRESENTATION OF SPINAL LESIONS SPINAL CORD LESIONS LOSS OF POWER BELOW THE LEVEL LOSS OF SENSATION BELOW THE LEVEL LOSS OF SPHINCTERIC CONTROL ROOT LESIONS PAIN ALONG A ROOT LOSS OF POWER IN A MUSCLE OR GROUP LOSS OF SENSATION IN A DERMATOME LOSS OF A REFLEX OR REFLEXES LOSS OF SPHINCTERIC CONTROL 08/18/12 FOURTH YEAR LECTURE 59
  • PRESENTATION OF SPINAL LESIONS ACUTE PRESENTATION  CHRONIC PRESENTATION  LOSS OF POWER  LOSS OF POWER  LOSS OF SENSATION  LOSS OF SENSATION  HYPOTONIA  HYPERTONIA  DECREASED REFLEXES  INCREASED REFLEXES  MUTE PLANTER REFLEX  EXTENSOR PLANTER REFLES ( BABINISKI) 08/18/12 FOURTH YEAR LECTURE 60
  • PRESENTATION OF CORD LESIONS EXAMPLE OF A SPINAL CORD LESION (TUMOUR) INTRADURAL SPINAL CORD TUMOR ON T2 WEIGHTED MRI08/18/12 FOURTH YEAR LECTURE 61
  • PRESENTATION OF ROOT LESIONS EXAMPLE OF A SPINAL ROOT LESION (PROLAPSED DISC) PROLAPSED DISC ON T1 WEIGHTED MRI08/18/12 FOURTH YEAR LECTURE 62