Dr. Rami Abo Ali

1. NEUROLOGY
Dr. Rami Abo Ali
Neurology
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Dr.
Rami
Abo
Ali
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2. INVESTIGATION OF NEUROLOGICAL DISEASE
PRESENTING PROBLEMS IN NEUROLOGICAL
DISEASE
Neurology
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Dr.
Rami
Abo
Ali
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3. INVESTIGATION OF NEUROLOGICAL
DISEASE
 Neuroimaging
 Plain X-rays
 Computed tomography (CT) ,CT angiography.
 Magnetic resonance (MR imaging (MRI), MR angiography
(MRA))
 Ultrasound (Doppler imaging of blood vessels)
 Nuclear medicine techniques
 Single photon emission computed tomography (SPECT) for
movement disorders, epilepsy, dementias
 Positron emission tomography (PET))
 Neurophysiological testing
 The electroencephalogram (EEG)
 Nerve conduction studies (NCS)
 Electromyography (EMG)
 Evoked potential studies
 Lumbar puncture
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Neurology
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Dr.
Rami
Abo
Ali

4. PLAIN X-RAYS
 Plain skull X-rays are now largely restricted to
the diagnosis of fractures and sinus disease.
 Plain X-rays of cervical, thoracic and lumbar spine are
useful in the investigation of trauma to vertebrae
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Neurology
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Dr.
Rami
Abo
Ali

5. COMPUTED TOMOGRAPHY (CT)
 Indications for Computed Tomography in Neurosurgery:
 Cranial CT:
1. Diagnosis of acute neurosurgical lesions in the head and
spine, including:
a. Skull and spinal fractures.
b. Intracranial hemorrhage: like extradural hematoma
,subdural hematoma, intracerebral hematoma.
2. Edema: brain edema whether due to trauma or other
cause.
3. Mass lesions: mainly brain mass lesions like tumours and
brain abscess.
4. Hydrocephalus
5. Stroke: differentiate between infarction and intracranial
hemorrhage. 5
Neurology
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Dr.
Rami
Abo
Ali

6.  Spinal CT:
1. Lumbar and cervical disc prolapse.
2. Lumbar and cervical canal stenosis.
3. Spinal trauma
4. Spinal dysraphism.
 Advantages :
 available, cheap and quick
 Disadvantages :
 Ionising radiation , contrast reactions , invasive
(myelography and angiography)
 Noncontrast CT misses many abnormalities
 Limited role in spinal pathology and contraindicated in
pregnancy unless performed as an emergency investigation.
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Dr.
Rami
Abo
Ali

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Dr.
Rami
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Ali

8. MAGNETIC RESONANCE IMAGING
 The Uses of the MRI
 Diagnosing: strokes; masses in soft tissue, infections
of the brain/spine/CNS
 Useful in the investigation of posterior fossa disease,
also visualizes temporal lobes in investigating
epilepsy.
 It effective in picking up inflammatory conditions
such as multiple sclerosis.
 MRI can also be applied to delineate arterial (MRA
for aneurysms) or venous anatomy (MRV for Cerebral
venous thrombosis CVT).
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Neurology
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Dr.
Rami
Abo
Ali

9.  Advantages
-No ionising radiation
-Non-invasive
- High-quality soft tissue images
- No bone artifact
 Disadvantages
-Expensive
-Less widely available
-Movement artifacts
-Severe claustrophobia (5%)
 Contraindications
•Implanted cardiac pacemakers
•Ferromagnetic aneurysm clips,
•Metallic implants
•Relatively contraindicated during the first trimester of
pregnancy leading to miscarriage. 9
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Dr.
Rami
Abo
Ali

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Ali

14. CT VS MRI
 MRI is better than CT in :
 In diagnoses of diseases related to soft tissues:
 Posterior fossa tumors (cerebellar and brain stem tumors).
 Spinal cord pathology (compression and tumors), and one can
do myelography with non invasive method (no need for lumbar
puncture).
 Infarction can be diagnosed as early as few hours whereas CT
needs 48 hours to diagnose it.
 No ionizing radiation.
 No bone artifact so that lesions around the skull base are
clearly identified.
 High resolution.
 CT is better than MRI in :
 Diagnoses of bone related pathologies like fractures and bone
tumors.
 Less time is needed to perform CT than MRI (few minutes) so CT
is better in irritable patients and critically ill patients.
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Neurology
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Dr.
Rami
Abo
Ali

15. ELECTROENCEPHALOGRAM (EEG)
 EEG is used to detect electrical activity arising in the
cerebral cortex.
 The EEG involves placing electrodes on the scalp to record
the amplitude and frequency of the resulting waveforms.
 EEG being performed during ictal and interictal phases. It
can be recorded with video monitoring.
 Over 50% of patients with proven epilepsy will have a
normal ‘routine’ EEG
 Up to 5% of some normal populations may demonstrate
epileptiform discharges on EEG
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Neurology
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Dr.
Rami
Abo
Ali

16.  The EEG is used in :
 Epilepsy classification and prognosis
 Localize the seat of epileptiform discharges when surgery is
being considered.
 Encephalopathy/encephalitis
 Sleep disorders
 Confirming brain death (not essential)
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Neurology
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Dr.
Rami
Abo
Ali

17. NERVE CONDUCTION STUDIES (NCS)
ELECTROMYOGRAPHY (EMG)
 Nerve conduction studies involve stimulating a nerve
with an electrical impulse via a surface electrode and
recording further along the nerve (sensory studies) or
recording the muscle action potential (motor studies)
 EMG involves the insertion of a needle electrode into
muscle. and electrical activity is recorded while the
muscle is contracting and resting.
 Denervated muscle fibers are recognized by increased
activity with needle insertion and abnormal spontaneous
activity (fibrillations and fasciculations)
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Neurology
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Dr.
Rami
Abo
Ali

18.  The Indications for these studies include:
1. Peripheral nerve injuries.
2. Peripheral nerve entrapment.
3. Brachial plexus injury.
4. Neuropathy.
5. Myopathy (studies are normal).
6. Muscular dystrophy (studies are normal).
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Neurology
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Dr.
Rami
Abo
Ali

19. EVOKED POTENTIALS
 Evoked potentials (EPs), or evoked responses,
measure the electrophysiologic responses of the
nervous system to a variety of stimuli.
 The EPs most frequently encountered are the
following:
 Visual evoked potentials (VEPs; these include both flash
and checkerboard types)
 Short-latency somatosensory evoked potentials (SEPs)
 Short-latency brainstem auditory evoked potentials
(BAEPs)
 MRI now provides more information about CNS
pathways, thus reducing reliance on EPs.
 In practice, visual evoked potentials (VEPs) are most
commonly used to help differentiate CNS
demyelination from small-vessel white-matter
changes 19
Neurology
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Dr.
Rami
Abo
Ali

20. LUMBAR PUNCTURE
 Lumbar puncture (LP) is the technique used to obtain both a CSF
sample and an indirect measure of intracranial pressure.
 After local anaesthetic injection, a needle is inserted between
lumbar spinous processes (usually between L3 and L4) through the
dura and into the spinal canal
 CSF pressure measurement is important in the diagnosis and
monitoring of idiopathic intracranial hypertension . In this
condition, the LP itself is therapeutic
 Routine analysis involves a cell count, as well as glucose and protein
concentrations.
 CSF assessment is important in investigating infections (meningitis
or encephalitis), subarachnoid hemorrhage and inflammatory
conditions (multiple sclerosis, sarcoidosis and cerebral lupus)
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Dr.
Rami
Abo
Ali

21.  Contraindications
 If there is any clinical suggestion of raised intracranial pressure
(papilloedema), depressed level of consciousness, or focal
neurological signs suggesting a cerebral lesion, until imaging (by
CT or MRI) has excluded a space-occupying lesion or
hydrocephalus
 If platelet count is less than 40,000 and Prothrombin time is less
than 50% of control
 LP can be safely performed in patients on antiplatelet drugs or
low-dose heparin, but may be unsafe in patients who are fully
anticoagulated due to the increased risk of epidural haematoma.
 About 30% of LPs are followed by a postural headache, due to
reduced CSF pressure. The frequency of headache can be
reduced by using smaller or atraumatic needles.
 Rarer complications involve transient radicular pain, and pain
over the lumbar region during the procedure. Aseptic technique
renders secondary infections such as meningitis extremely rare.
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Dr.
Rami
Abo
Ali

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Dr.
Rami
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Ali

23. BIOPSY
 Biopsies of nervous tissue (peripheral nerve, muscle,
meninges or brain) are occasionally required for diagnosis.
 Nerve biopsy can help in the investigation of peripheral
neuropathy. Usually, a distal sensory nerve (sural or
radial) is targeted.
 Muscle biopsy is performed more frequently and is
indicated for the differentiation of myositis and myopathies
 Most brain biopsies are performed stereotactically through
a burr hole in the skull, which lowers complication rates.
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Neurology
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Dr.
Rami
Abo
Ali

24. PRESENTING PROBLEMS IN NEUROLOGICAL DISEASE
 LOSS OF CONSCIOUSNESS
 Syncope
 Coma
 ALTERATION IN BEHAVIOR
 Delirium
 Dementia
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Dr.
Rami
Abo
Ali

25. SYNCOPE
 Definition :
 Syncope refers to a transient loss of consciousness
that typically follows insufficient blood supply to the
brain for more than a few seconds
 Clinical signs :
 Patients are transiently unresponsive, with
diminished muscle tone. A few generalized tonic
spasms may occur, especially if patients are
prevented from lying down.
 Etiology :
 Most patients with syncope have a cardiac or
circulatory basis for the event, although neurologic
conditions need to be considered if the diagnosis
remains elusive 25
Neurology
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Dr.
Rami
Abo
Ali

26. SYNCOPE
ETIOLOGY
 Circulatory disturbances are particularly common.
 Vasovagal syncope, which is often seen in young people, is
commonly associated with emotional stress, fear, or pain.
 Postprandial syncope , which frequently affects the elderly,
often occurs following meals in which alcohol has been
consumed.
 Syncope can occur in diverse settings that have in common
a preceding Valsalvaor straining maneuver that decreases
venous return and promotes parasympathetic tone (e.g.,
micturition syncope).
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Neurology
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Dr.
Rami
Abo
Ali

27. SYNCOPE
ETIOLOGY
 Cardiac output disturbances , other than arrhythmia
or mechanical obstruction, should be considered.
a) Vasodepressor (neurocardiogenic) syncope is caused by
undue stimulation of afferent cardiac mechanoreceptors
because of cardiac distention or strenuous contractions.
This causes a decrease in sympathetic activity and an
increase in parasympathetic activity that leads to
vasodilation, bradycardia, and subsequent hypotension.
b) Carotid sinus hypersensitivity can lead to
bradyarrhythmias and hypotension. Because carotid
sinus hypersensitivity is present in many older men, it
should be considered responsible for syncope only if
other causes have been excluded
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Neurology
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Dr.
Rami
Abo
Ali

28. SYNCOPE
ETIOLOGY
 Neurologic disorders are relatively uncommon causes of
syncope. Several conditions are important because they
can lead to unresponsiveness and are therefore often
considered during the evaluation of a patient with
transient unresponsiveness.
 Seizures are a cause of unresponsiveness that must be
differentiated from syncope.
a) Patients are rarely limp during seizures. Many seizures
cause sustained limb extension (tonic activity) or
intermittent, relatively rhythmic limb contractions (clonic
activity).
b) Atonic seizures are rare in adults but do cause sudden
collapse. Absence seizures, conversely, do not result in falls.
c) Because some patients with syncope can exhibit
involuntary movements, the possibility of a primary seizure
is a consideration. However, in most cases, the tonic or
myoclonic activity tends to occur several seconds after
consciousness is lost and merely reflects cerebral
hypoperfusion, not a primary seizure disorder.
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Neurology
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Dr.
Rami
Abo
Ali

29. SYNCOPE
ETIOLOGY
 Subarachnoid hemorrhage (SAH) can transiently
increase intracranial pressure (ICP), compromising
global cerebral perfusion. Clues to the diagnosis
include persistent, severe headache, meningismus,
and papilledema.
 Basilar artery migraine (a unique type of migraine
with aura) is a rare cause of unresponsiveness. A
history of recurrent headache, recurrent episodes of
unresponsiveness, and associated symptoms (e.g.,
visual distortion and dizziness) should lead to
consideration of this condition
 Narcolepsy ( sleep disorder )can cause episodes of
sleep or cataplexy (loss of tone) that can be mistaken
for syncope. 29
Neurology
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Dr.
Rami
Abo
Ali

30. SYNCOPE
ETIOLOGY
 Hypoglycemia causes a lack of nutrient supply to
the brain and can lead to syncope. Hypoglycemia
as a cause of syncope is particularly likely in
patients with type 1 (insulin-dependent)
diabetes. Therapy involves the administration of
glucose.
 Psychogenic unresponsiveness can be associated
with anxiety, panic attacks, or hyperventilation,
as well as somatoform (conversion) disorder. In
this case findings on the exam should allow one
to confirm consciousness
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Dr.
Rami
Abo
Ali

31. SYNCOPE
DIAGNOSIS & THERAPY
 A history and physical examination often can provide
clues to the proper diagnosis.
 If no clues are evident, it is generally appropriate to
proceed with a cardiovascular evaluation
a) Neurologic testing frequently includes an EEG. Rarely is
a CT scan diagnostic. In some patients, an MRI or an
imaging study of the vascular system can be informative.
b) Upright tilt testing, possibly with isoproterenol infusion,
can provide evidence for a diagnosis of vasodepressor
(neurocardiogenic) syncope, especially if the
characteristic hemodynamic changes occur in less than
15 minutes without isoproterenol infusion.
 Therapy.:
 Treatment depends on the underlying diagnosis
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Neurology
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Dr.
Rami
Abo
Ali

32. COMA
 Definition.
 Coma is a state in which a patient is unconscious and
unresponsive to environmental stimuli.
 Coma is associated with extensive structural or
physiologic damage to both cerebral hemispheres or
to the ascending reticular activating system in the
brainstem.
 In practice, this means a sustained Glasgow Coma
Scale (GCS) of 8 or less
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35. COMA
APPROACH TO THE PATIENT
 Complete and rapid assessment is critical for optimal
care.
 The physician should ascertain the time of onset of
the loss of consciousness, as well as the following
information from someone close to the patient:
a) Past medical history ,especially of a preexisting
neurologic, cardiac, pulmonary, hepatic, or renal
condition
b) Prescription and over-the-counter drugs used by the
patient
c) History of drug abuse if applicable
d) Recent patient complaints
e) Details regarding the site where the patient was found
(e.g., presence of empty drug vials, evidence of a fall) 35
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Rami
Abo
Ali

36. COMA
PHYSICAL EXAMINATION
 The examination should be thorough.
 Extremes of blood pressure, pulse, or temperature,
abnormal breathing patterns, evidence of head or
neck trauma, and the presence of meningismus
should be noted carefully.
 The skin should be inspected for signs of trauma or
needle tracks.
 Special attention should be directed to the following:
 Pupils
 Ocular motility
 Motor functions
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Dr.
Rami
Abo
Ali

37. COMA
PHYSICAL EXAMINATION
 Pupils :
 Pupillary size and reactivity are dependent on
sympathetic and parasympathetic innervation .
Brainstem reflexes such as the pupillary reaction to
light offer clues to the location of the lesion responsible
for the coma.
a) Large, nonreactive pupils result from the disruption
of the parasympathetic portion of the third cranial
nerve but may also be seen with barbiturate
overdose.
b) Small, reactive pupils result from the disruption of
the sympathetic pupillodilatory impulses that arise
in the hypothalamus and course caudally through
the periaqueductal gray matter and cervical spinal
cord before traveling with the internal carotid
artery toward the eyes.
c) Pinpoint pupils that are nonreactive to light may be
seen with narcotic overdose
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Dr.
Rami
Abo
Ali

38.  Ocular motility.
 Analysis of ocular motility allows assessment of damage to
the brainstem and the cranial nerves that control eye
movement.
a) The eyes should first be examined in the resting position
for spontaneous motion of the eyeballs. Although the eyes
of comatose patients may move spontaneously, they do
not fixate or track in a purposeful manner.
b) If the eyes are immobile, movement can be elicited
through the vestibulo-ocular reflex by moving the
patient’s head side to side (the “doll’s eyes ” or
oculocephalic maneuver) or by elevating the patient’s
head 30 degrees and irrigating the external auditory
canal with ice water (i.e., cold caloric testing). The former
should only be performed after a cervical injury is ruled
out.
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Neurology
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Dr.
Rami
Abo
Ali
COMA
PHYSICAL EXAMINATION

39.  Conjugate deviation of the eyes bilaterally toward the
cold water implies intact brainstem circuitry.
 Failure of an eye to abduct in response to these
maneuvers implies sixth nerve compromise.
 Failure of an eye to adduct implies dysfunction of the
medial longitudinal fasciculus or oculomotor nucleus or
nerve.
 Failure of either eye to respond implies an ipsilateral
pontine lesion.
 The presence of conjugate nystagmus away from the side
of ice water irrigation suggests psychogenic coma
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Dr.
Rami
Abo
Ali
COMA
PHYSICAL EXAMINATION

40. COMA
PHYSICAL EXAMINATION
 Motor functions :
 Quadriparesis , hemiparesis , or monoparesis
may occur in comatose patients.
 Quadriparesis and flaccidity suggest pontine or
medullary compromise or a high cervical spinal cord
insult.
 Decorticate posturing(i.e., leg extension with flexion
of the arm, wrist, and fingers) can be unilateral or
bilateral and suggests a hemispheric or diencephalic
lesion.
 Decerebrate posturing(i.e., leg and arm extension)
also can be unilateral or bilateral and suggests
midbrain or pontine compromise 40
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Dr.
Rami
Abo
Ali

41. COMA
CLINICAL FEATURES
 Once global brainstem dysfunction has developed,
differentiation between supratentorial and
infratentorial causes of coma cannot be made without
diagnostic testing unless a history and serial
observations of the patient’s clinical course can be
documented.
 Supratentorial causes of coma are often characterized
by pathologic processes that result in swelling of a
cerebral hemisphere.
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Rami
Abo
Ali

42. 1) This mass effect causes a midline shift of the
affected hemisphere toward the contralateral side,
compression of the ipsilateral third nerve as it
courses near the medial temporal lobe (uncus),
herniation of the medial temporal lobe below the
tentorial notch (uncal herniation), distortion of the
mesencephalon, and herniation of the cingulate
gyrus under the midline falx (subfalcial herniation).
2) Typically, there is a progressive clinical
deterioration characterized by increasing
unresponsiveness, development of a third nerve
palsy ipsilateral to the swollen hemisphere, and,
ultimately, midbrain compromise (reflected by
bilaterally nonreactive, dilated pupils).
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Dr.
Rami
Abo
Ali
COMA
CLINICAL FEATURES

43.  Infratentorial causes of coma can be suspected if
ataxia, multiple asymmetric cranial nerve palsies, and
unilateral or bilateral limb weakness or sensory loss
develop before the development of more global, severe
impairment of brainstem function (characterized by
nonreactive pupils, absent ocular motility, and absent
corneal and gag reflexes).
 Diffuse, toxic, or metabolic causes of coma can be
suspected if pupillary responses are intact, ocular
motility is preserved, corneal reflexes can be elicited, a
gag reflex is present, and limb movement in response to
noxious local stimuli is observed. If pupillary
responsiveness persists in the absence of other
brainstem and limb function, a metabolic cause of coma
should be considered.
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Dr.
Rami
Abo
Ali
COMA
CLINICAL FEATURES

44.  Psychogenic coma should be suspected if the
patient has a history of psychiatric disease or if
the findings on physical examination are
nonphysiologic. Examples of nonphysiologic
responses in a “comatose” patient include the
following:
a) The presence of nystagmus when the patient’s ears
are irrigated with ice water
b) Adversive head and eye movements
c) Failure of the patient’s arm, when held by the
examiner over the patient’s face, to fall towards the
face when released by the examiner
d) Resistance to having the eyelids opened
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Dr.
Rami
Abo
Ali
COMA
CLINICAL FEATURES

45.  Initial therapy :
 The “ABCs”: Maintaining an adequate airway, optimal
ventilation, and appropriate blood pressure are priority
concerns.
 If cervical fracture is a possibility, immobilization of the
neck is of great importance.
 Endotracheal intubation may be indicated to protect the
airway.
 Blood samples for a complete blood count (CBC),
electrolytes, glucose, renal and liver function studies,
coagulation profiles, blood gases, and toxicology should
be obtained.
 Intravenous thiamine(100 mg), one ampule of dextrose
50% in water (D50W),and naloxone(0.4 mg) are often
administered. Flumazenil can be given if
benzodiazepine or hepatic coma is suspected.
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Dr.
Rami
Abo
Ali
COMA
TREATMENT

46.  Imaging:
 If the patient’s general medical condition
permits, and if the cause of coma is not clearly
cerebral anoxia after cardiopulmonary arrest or a
drug overdose, most patients should have a brain
CT scan to define the presence of an intracranial
mass, cerebral edemaor hydrocephalus .
 Further management depends on the etiology of
the coma.
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Neurology
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Dr.
Rami
Abo
Ali
COMA
TREATMENT

47.  ICP (intracranial pressure) evaluation and
management
 ICP evaluation : Consideration of the patient’s ICP is
intimately tied to the evaluation of coma.
 The intracranial cavity has a finite volume and
compliance.
 Normally, modest volume additions to the intracranial
contents (e.g., from a small intraparenchymal
hematoma) cause only a small rise in ICP.
 With progressive incremental increases to the
intracranial volume (e.g., from massive cerebral
edema, a hematoma, or a tumor), the intracranial
compliance decreases and the ICP markedly increases.
 Because cerebral perfusion pressure is the result of
the mean arterial pressure minus the ICP, an
excessive rise of the ICP is associated with impaired
cerebral perfusion and progressive neurologic
deterioration.
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Rami
Abo
Ali
COMA
TREATMENT

48.  ICP management:
 If a pathologic process associated with elevated ICP is
suspected, emergency management should include steps to
decrease the pressure or, at the very least, avoid increasing it.
 If possible, the cerebral perfusion pressure (CPP), where CPP
mean arterial pressure (MAP) – ICP, should be kept at greater
than 60 mm Hg and the ICP at less than 20 mm Hg.
 Optimal management of increased ICP often requires direct ICP
monitoring, as well as determination of hemodynamic
parameters.
 Patients can be hyperventilated with an Ambu bag before
intubation. Intubation and endotracheal suctioning should be
performed carefully to minimize elevation of ICP.
 Fever and agitation should be minimized.
 The patient’s head should be elevated 30 degrees and kept in
midposition to optimize venous drainage.
 Osmotic therapy is used to dehydrate the brain and decrease the
ICP. Patients are kept euvolemic , and intravenous mannitol or
hypertonic saline is administered to achieve a hyperosmotic state.
 Durotomy and hemicraniectomy can be used to decompress swollen
brain.
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Dr.
Rami
Abo
Ali
COMA
TREATMENT

49.  The prognosis of coma is generally related to the
cause of the coma, the depth of the coma, and the
duration.
 In one series, the probability of good or moderate
recovery was only 2% once the patient had
remained in coma for 14 days.
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Rami
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COMA
PROGNOSIS

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Rami
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Ali