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Care in specialized intensive care units (ICUs) is generally of
higher quality than in general care units. Neurocritical care
focuses on the care of critically ill patients with primary or
secondary neurosurgical and neurological problems and was
initially developed to manage postoperative neurosurgical
patients. It expanded thereafter to the management of patients
with traumatic brain injury (TBI), intracranial hemorrhage and
complications of subarachnoid hemorrhage; including
vasospasm, elevated intracranial pressure (ICP) and the
cardiopulmonary complications of brain injury.
Neurocritical care units have developed to coordinate the
management of critically ill neurological patients in a single
specialized unit, which includes many clinical domains. Care is
provided by a multidisciplinary team trained to recognize and
deal with the unique aspects of the neurological disease
processes, as several treatable neurological disorders are
characterized by imminent risk of severe and irreversible
neurological injury or death if treatment is delayed.
Some diseases need immediate action, so admission to the NICU
is the best solution when there is:
higher quality than in general care units. Neurocritical care
focuses on the care of critically ill patients with primary or
secondary neurosurgical and neurological problems and was
initially developed to manage postoperative neurosurgical
patients. It expanded thereafter to the management of patients
with traumatic brain injury (TBI), intracranial hemorrhage and
complications of subarachnoid hemorrhage; including
vasospasm, elevated intracranial pressure (ICP) and the
cardiopulmonary complications of brain injury.
Neurocritical care units have developed to coordinate the
management of critically ill neurological patients in a single
specialized unit, which includes many clinical domains. Care is
provided by a multidisciplinary team trained to recognize and
deal with the unique aspects of the neurological disease
processes, as several treatable neurological disorders are
characterized by imminent risk of severe and irreversible
neurological injury or death if treatment is delayed.
Some diseases need immediate action, so admission to the NICU
is the best solution when there is:
1) Impaired level of consciousness.
2) Progressive respiratory impairment or the need for
mechanical ventilation in a neurological patient.
3) Status epilepticus or prolonged seizures.
4) Clinical or Computed Tomographic (CT) evidence of raised
Intracranial Pressure (ICP), whatever the cause (space
occupying lesion, cerebral edema or hemorrhagic
conversion of a cerebral infarct, intracerebral hemorrhage,
etc.)
5) Need for monitoring (for example, level of consciousness,
ICP, continuous electroencephalography (cEEG)), and
6) Need for specific treatments (Baldwin 2010) (e.g.,
neurosurgery, intravenous or arterial thrombolysis).
In the Neurocritical Care unit, patients with primary
neurological diseases such as myasthenia gravis, Guillain-Barré
syndrome, status epilepticus, and stroke have a better outcome
than those patients with secondary neurological diseases. So, we
can conclude that these specialized units have greater
experience in the anticipation, early recognition, and
management of potentially fatal complications.
Early identification of patients at risk of life threatening
neurological illness in order to manage them properly and to
prevent further deterioration is the role of general assessment of
new patients in a neurological emergency. History taking and a
rapid neurological assessment of a specific patient in specialized
neurocritical care units helps answer the question ‘how sick is
this patient?’.
The neurologic screening examination in the emergency
settings focuses primarily on identifying acute, potentially lifethreatening
processes, and secondarily on identifying disorders
that require other opinions, of other specialists.
The importance of urgent neurologic assessment comes from
recent advances in the management of neurologic disorders
needing timely intervention like thrombolysis in acute ischemic
2) Progressive respiratory impairment or the need for
mechanical ventilation in a neurological patient.
3) Status epilepticus or prolonged seizures.
4) Clinical or Computed Tomographic (CT) evidence of raised
Intracranial Pressure (ICP), whatever the cause (space
occupying lesion, cerebral edema or hemorrhagic
conversion of a cerebral infarct, intracerebral hemorrhage,
etc.)
5) Need for monitoring (for example, level of consciousness,
ICP, continuous electroencephalography (cEEG)), and
6) Need for specific treatments (Baldwin 2010) (e.g.,
neurosurgery, intravenous or arterial thrombolysis).
In the Neurocritical Care unit, patients with primary
neurological diseases such as myasthenia gravis, Guillain-Barré
syndrome, status epilepticus, and stroke have a better outcome
than those patients with secondary neurological diseases. So, we
can conclude that these specialized units have greater
experience in the anticipation, early recognition, and
management of potentially fatal complications.
Early identification of patients at risk of life threatening
neurological illness in order to manage them properly and to
prevent further deterioration is the role of general assessment of
new patients in a neurological emergency. History taking and a
rapid neurological assessment of a specific patient in specialized
neurocritical care units helps answer the question ‘how sick is
this patient?’.
The neurologic screening examination in the emergency
settings focuses primarily on identifying acute, potentially lifethreatening
processes, and secondarily on identifying disorders
that require other opinions, of other specialists.
The importance of urgent neurologic assessment comes from
recent advances in the management of neurologic disorders
needing timely intervention like thrombolysis in acute ischemic
stroke, anticonvulsants for nonconvulsive and subtle generalized
status epilepticus, and plasmapheresis for Guillain-Barré, etc.
It is obvious that interventions can be time-sensitive and can
significantly reduce morbidity and mortality.
A comprehensive neurologic screening assessment can be
accomplished within minutes if performed in an organized and
systematic manner (Goldberg 1987). Neurologic screening
assessment includes six major components of the neurologic
exam, namely:
1) Mental status
2) Cranial nerve exam
3) Motor exam
4) Reflexes
5) Sensory exam
6) Evaluation of coordination and balance.
Based on the chief findings of the screening assessment,
further evaluation or investigations can be then decided upon.
History
A careful history is the first step to successful diagnosis, and
then intervention. Careful history provides clues to the
pathology of the patient’s condition, and may help direct the
diagnostic workup. For example, an alert patient with a
headache associated with neck pain that started after a car
accident might help direct the examination and radiographic
imaging to focus on cervical spine injury or neck vessels (carotid
or vertebral artery) dissection, while the same patient not in a
car accident may direct your attention to a spontaneous
subarachnoid hemorrhage.
The history begins with a definition of the patient’s complaint,
but aiming at determining key points: time and mode of onset,
mode of progression, associated symptoms, and a prior history
of similar conditions. Dramatic or acute onset of neurologic
events suggests a vascular insult and mandates immediate
attention and intervention.
status epilepticus, and plasmapheresis for Guillain-Barré, etc.
It is obvious that interventions can be time-sensitive and can
significantly reduce morbidity and mortality.
A comprehensive neurologic screening assessment can be
accomplished within minutes if performed in an organized and
systematic manner (Goldberg 1987). Neurologic screening
assessment includes six major components of the neurologic
exam, namely:
1) Mental status
2) Cranial nerve exam
3) Motor exam
4) Reflexes
5) Sensory exam
6) Evaluation of coordination and balance.
Based on the chief findings of the screening assessment,
further evaluation or investigations can be then decided upon.
History
A careful history is the first step to successful diagnosis, and
then intervention. Careful history provides clues to the
pathology of the patient’s condition, and may help direct the
diagnostic workup. For example, an alert patient with a
headache associated with neck pain that started after a car
accident might help direct the examination and radiographic
imaging to focus on cervical spine injury or neck vessels (carotid
or vertebral artery) dissection, while the same patient not in a
car accident may direct your attention to a spontaneous
subarachnoid hemorrhage.
The history begins with a definition of the patient’s complaint,
but aiming at determining key points: time and mode of onset,
mode of progression, associated symptoms, and a prior history
of similar conditions. Dramatic or acute onset of neurologic
events suggests a vascular insult and mandates immediate
attention and intervention.
Physical Exam
1. Mental status
Usually we start neurologic examination by assessing the
patient’s mental status (Strub 2000).
A full mental status exam is not necessary in the patient who is
conscious, awake, oriented, and conversant; on the contrary it
must be fully investigated in patients with altered mental status.
Sometimes, we can find no change in mental status; at that
point careful consideration should be given to concerns of
family.
A systematic approach to the assessment of mental status is
helpful in detecting acute as well as any chronic disease, such as
delirious state in a demented patient (Lewis 1995). The CAM
(confusion assessment method) score was developed to assist in
diagnosing delirium in different contexts. CAM assesses four
components: acute onset, inattention, disorganized thinking or
an altered level of consciousness with a fluctuating course. A
‘Mini-Mental Status’ test can also be used but usually is reserved
for patients with suspected cognitive dysfunction as it evaluates
five domains – orientation, registration, attention, recall, and
language (Strub 2000).
2. Cranial nerve (CN) exam
Cranial Nerves II - VIII function testing are of utmost value in the
neurologic assessment in an emergency setting (Monkhouse
2006).
Cranial Nerves II – Optic nerve assessment involves visual
acuity and fields, along with a fundus exam and a swinging
flashlight test. Visual field exam using the confrontation method
is rapid and reliable. Visual loss in one eye suggests a nerve
lesion, i.e., in front of the chiasm; bitemporal hemianopsia
suggests a lesion at the optic chiasm; a quadrant deficit suggests
a lesion in the optic tracts; bilateral visual loss suggests cortical
disease.
1. Mental status
Usually we start neurologic examination by assessing the
patient’s mental status (Strub 2000).
A full mental status exam is not necessary in the patient who is
conscious, awake, oriented, and conversant; on the contrary it
must be fully investigated in patients with altered mental status.
Sometimes, we can find no change in mental status; at that
point careful consideration should be given to concerns of
family.
A systematic approach to the assessment of mental status is
helpful in detecting acute as well as any chronic disease, such as
delirious state in a demented patient (Lewis 1995). The CAM
(confusion assessment method) score was developed to assist in
diagnosing delirium in different contexts. CAM assesses four
components: acute onset, inattention, disorganized thinking or
an altered level of consciousness with a fluctuating course. A
‘Mini-Mental Status’ test can also be used but usually is reserved
for patients with suspected cognitive dysfunction as it evaluates
five domains – orientation, registration, attention, recall, and
language (Strub 2000).
2. Cranial nerve (CN) exam
Cranial Nerves II - VIII function testing are of utmost value in the
neurologic assessment in an emergency setting (Monkhouse
2006).
Cranial Nerves II – Optic nerve assessment involves visual
acuity and fields, along with a fundus exam and a swinging
flashlight test. Visual field exam using the confrontation method
is rapid and reliable. Visual loss in one eye suggests a nerve
lesion, i.e., in front of the chiasm; bitemporal hemianopsia
suggests a lesion at the optic chiasm; a quadrant deficit suggests
a lesion in the optic tracts; bilateral visual loss suggests cortical
disease.
Assessment of the optic disc, retinal arteries, and retinal veins
can be done by a fundus exam, to discover papilledema, flame
hemorrhages or sheathing.
Cranial Nerves III, IV, VI – CN III innervates the extraocular
muscles for primarily adduction and vertical gaze. CN III
function is tested in conjunction with IV, which aids in internal
depression via the superior oblique, and VI, which controls
abduction via the lateral rectus. Extraocular muscle function is
tested for diplopia, which requires binocular vision and thus will
resolve when one eye is occluded. Marked nystagmus on lateral
gaze or any nystagmus on vertical gaze is abnormal; vertical
nystagmus is seen in brainstem lesions or intoxication, while
pendular nystagmus is generally a congenital condition.
The pupillary light reflex is mediated via the parasympathetic
nerve fibers running on the outside of CN III. In the swinging
flashlight test a light is shone from one eye to the other; when
the light is shone directly into a normal eye, both eyes constrict
via the direct and the consensual light response.
Pupillary size must be documented. Asymmetry in pupils of less
than 1 mm is not significant. Significant difference in pupil size
suggests nerve compression due to aneurysms or due to cerebral
herniation, in patients with altered mental status.
Bilateral pupillary dilation is seen with prolonged anoxia or
due to drugs (anticholinergics), while bilateral pupillary
constriction is seen with pontine hemorrhage or as the result of
drugs (e.g., opiates, clonidine).
Cranial Nerve V – Individual branch testing of the trigeminal
nerve is unnecessary, as central nervous system lesions affecting
CN V usually involve all three branches.
Cranial Nerve VII – The facial nerve innervates motor
function to the face, and sensory function to the ear canal, as
well as to the anterior two-thirds of the tongue. Central lesions
cause contralateral weakness of the face muscles below the eyes.
Cranial Nerve VIII – The acoustic nerve has a vestibular and a
cochlear component. An easy screening test for hearing defects
is accomplished by speaking in graded volumes to the patient.
18
can be done by a fundus exam, to discover papilledema, flame
hemorrhages or sheathing.
Cranial Nerves III, IV, VI – CN III innervates the extraocular
muscles for primarily adduction and vertical gaze. CN III
function is tested in conjunction with IV, which aids in internal
depression via the superior oblique, and VI, which controls
abduction via the lateral rectus. Extraocular muscle function is
tested for diplopia, which requires binocular vision and thus will
resolve when one eye is occluded. Marked nystagmus on lateral
gaze or any nystagmus on vertical gaze is abnormal; vertical
nystagmus is seen in brainstem lesions or intoxication, while
pendular nystagmus is generally a congenital condition.
The pupillary light reflex is mediated via the parasympathetic
nerve fibers running on the outside of CN III. In the swinging
flashlight test a light is shone from one eye to the other; when
the light is shone directly into a normal eye, both eyes constrict
via the direct and the consensual light response.
Pupillary size must be documented. Asymmetry in pupils of less
than 1 mm is not significant. Significant difference in pupil size
suggests nerve compression due to aneurysms or due to cerebral
herniation, in patients with altered mental status.
Bilateral pupillary dilation is seen with prolonged anoxia or
due to drugs (anticholinergics), while bilateral pupillary
constriction is seen with pontine hemorrhage or as the result of
drugs (e.g., opiates, clonidine).
Cranial Nerve V – Individual branch testing of the trigeminal
nerve is unnecessary, as central nervous system lesions affecting
CN V usually involve all three branches.
Cranial Nerve VII – The facial nerve innervates motor
function to the face, and sensory function to the ear canal, as
well as to the anterior two-thirds of the tongue. Central lesions
cause contralateral weakness of the face muscles below the eyes.
Cranial Nerve VIII – The acoustic nerve has a vestibular and a
cochlear component. An easy screening test for hearing defects
is accomplished by speaking in graded volumes to the patient.
18
When vestibular nerve defects are suspected, patients are
assessed for nystagmus, via a past-pointing test and a positive
response to the Nylen-Barany maneuver.
3. Motor exam
Motor system assessment focuses on detecting asymmetric
strength deficits, which may indicate an acute CNS lesion.
Testing motor power can be difficult or impossible in the
uncooperative patient. It is not mandatory to test different
muscle groups but instead just test for the presence of a “drift”.
In diseased patients, the hand and arm on the affected side will
slowly drift or pronate when they try to hold their arm out
horizontally, palms up with eyes closed.
4. Reflexes
For rapid assessment of reflexes, major deep tendon reflexes and
the plantar reflex must be elicited. Major deep tendon reflexes
include the patellar reflex, the Achilles reflex, the biceps reflex,
and the triceps reflex. Response can be graded from 0 (no reflex)
to 4+ (hyperreflexia). Asymmetrical reflexes are the most
important as they are considered pathologic. Many reflexes
indicate upper motor neuron disease; the most commonly
elicited is Babinski’s reflex.
5. Sensory exam
For rapid assessment of the sensory system, pain and light touch
sensations should be done. Testing for other sensory modalities
is reserved for patients with suspected neuropathies or for
further evaluation of sensory complaints.
6. Coordination and balance
Coordination depends on functional integration of the
cerebellum and sensory input from vision, proprioception, and
the vestibular sense. Coordination assessment is an important
part of neurological assessment, as many central lesions may
present only with coordination disturbance, such as cerebellar
infarction, hemorrhage or cerebellar connections insult.
assessed for nystagmus, via a past-pointing test and a positive
response to the Nylen-Barany maneuver.
3. Motor exam
Motor system assessment focuses on detecting asymmetric
strength deficits, which may indicate an acute CNS lesion.
Testing motor power can be difficult or impossible in the
uncooperative patient. It is not mandatory to test different
muscle groups but instead just test for the presence of a “drift”.
In diseased patients, the hand and arm on the affected side will
slowly drift or pronate when they try to hold their arm out
horizontally, palms up with eyes closed.
4. Reflexes
For rapid assessment of reflexes, major deep tendon reflexes and
the plantar reflex must be elicited. Major deep tendon reflexes
include the patellar reflex, the Achilles reflex, the biceps reflex,
and the triceps reflex. Response can be graded from 0 (no reflex)
to 4+ (hyperreflexia). Asymmetrical reflexes are the most
important as they are considered pathologic. Many reflexes
indicate upper motor neuron disease; the most commonly
elicited is Babinski’s reflex.
5. Sensory exam
For rapid assessment of the sensory system, pain and light touch
sensations should be done. Testing for other sensory modalities
is reserved for patients with suspected neuropathies or for
further evaluation of sensory complaints.
6. Coordination and balance
Coordination depends on functional integration of the
cerebellum and sensory input from vision, proprioception, and
the vestibular sense. Coordination assessment is an important
part of neurological assessment, as many central lesions may
present only with coordination disturbance, such as cerebellar
infarction, hemorrhage or cerebellar connections insult.
By the end of the examination, you should reach a clinical
diagnosis, which includes answers to the two critical questions,
what is the lesion? and where is the lesion?
7. Neuroanatomical localization
Some knowledge of neuroanatomy is essential for correct
localization. The first step in localizing neurological lesions
should be to determine if it is a central (upper motor neuron)
lesion (i.e., in the brain or spinal cord) versus a peripheral (lower
motor neuron) lesion (i.e., nerve or muscle).
The hallmark of upper motor neuron lesions is hyperreflexia
with or without increased muscle tone. Central (upper motor
neuron) lesions are localized to:
Brain
– Cortical brain (frontal, temporal, parietal, or occipital lobes)
– Subcortical brain structures (corona radiata, internal
capsule, basal ganglia, or thalamus)
– Brainstem (medulla, pons, or midbrain)
– Cerebellum
Spinal cord
– Cervicomedullary junction
– Cervical
– Thoracic
– Upper lumbar
The hallmark of a lower motor neuron (LMN) lesion is
decreased muscle tone, leading to flaccidity and hyporeflexia.
Peripheral LMN lesions are localized to:
– Anterior horn cells
– Nerve root(s)
– Plexus
– Peripheral nerve
– Neuromuscular junction
– Muscle
diagnosis, which includes answers to the two critical questions,
what is the lesion? and where is the lesion?
7. Neuroanatomical localization
Some knowledge of neuroanatomy is essential for correct
localization. The first step in localizing neurological lesions
should be to determine if it is a central (upper motor neuron)
lesion (i.e., in the brain or spinal cord) versus a peripheral (lower
motor neuron) lesion (i.e., nerve or muscle).
The hallmark of upper motor neuron lesions is hyperreflexia
with or without increased muscle tone. Central (upper motor
neuron) lesions are localized to:
Brain
– Cortical brain (frontal, temporal, parietal, or occipital lobes)
– Subcortical brain structures (corona radiata, internal
capsule, basal ganglia, or thalamus)
– Brainstem (medulla, pons, or midbrain)
– Cerebellum
Spinal cord
– Cervicomedullary junction
– Cervical
– Thoracic
– Upper lumbar
The hallmark of a lower motor neuron (LMN) lesion is
decreased muscle tone, leading to flaccidity and hyporeflexia.
Peripheral LMN lesions are localized to:
– Anterior horn cells
– Nerve root(s)
– Plexus
– Peripheral nerve
– Neuromuscular junction
– Muscle
Conclusions
1. The neurological screening examination provides the
clinician with the necessary data to make management
decisions.
2. A cranial nerve examination gives plenty of data in the
emergency setting and is a critical component of the
screening exam
1. The neurological screening examination provides the
clinician with the necessary data to make management
decisions.
2. A cranial nerve examination gives plenty of data in the
emergency setting and is a critical component of the
screening exam
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