BIOLOGICAL BASIS OF BEHAVIOR
Psychology 321
Spring, 2005 HGH 225
Dr. John M. Morgan MWF, 8am to 9:00
Brainstem Lesions and Tumors
James Eubanks and Jeff Slocum
James Eubanks Professor Morgan
Brainstem Injuries and the Neuropsychologist
The Neuropsychologist plays an essential function in assessment
and rehabilitation after an injury to the head.
Neuropsychologists essentially bear responsibility for testing
and tracking the patients thinking ability. Below are key
functions provided by clinical neuropsychologists:
? Carrying out detailed assessments of cognition, emotion,
behavior, and social competence;
? Devising and implementing training programs;
? Liaising with educational agencies/ employers to advise on
the resumption of educational/ vocational life;
? Advising on the management cognitive deficits/
disabilities;
? Advising and providing long term care;
? Providing psychotherapeutic input to address the emotional
impact of injury and disabilities;
? Facilitating personal, family, and social adjustment
(Halligan 2003).
A screening for a neuropsychological evaluation should be done
as soon as possible after an injury to the brain or in this
case, brainstem. A comprehensive evaluation is necessary if
complaints and or problems persist. In most cases, an evaluation
is performed biannually for the first two years, and as
necessary, depending on the subjectivity of the patients status.
An exam by the neuropsychologist typically involves a wide
variety of tasks, most of which are done sitting at a table or
at bedside in a hospital (www.neuropsychologycentral.com, 2002).
The examination is non-invasive, and usually is not painful. The
evaluation often takes 6 to 8 hours of face-to-face contact, but
can vary widely depending on what information is being sought
(www.neuropsychologycentral.com, 2002).
Test results are used, depending on the reason for the
evaluation. In this case, we are studying lesions or tumors to
the brainstem:
? Confirm or clarify a diagnosis.
? Provide a profile of strengths and weaknesses to guide
rehabilitation, educational, vocational, or other services.
? Document changes in functioning since prior examinations,
including effects of treatment.
? Clarify what compensatory strategies would help.
? Result in referrals to other specialists, such as
educational therapists, cognitive rehabilitation
professionals, neurologists, psychiatrists, psychologists,
social workers, nurses, special education teachers, or
vocational counselors (www.neuropsychologycentral.com,
2005).
Neuropsychologists evaluate and monitor the course of recovery
or the efficiency of rehabilitation. And the big question Is the
person getting better? A Neuropsychological evaluation may be
essential to verify whether a person really has a brainstem
injury. The effects of stress, medications, and or depression
can be easily confused with mild brain injury. Some research
indicates that neuropsychologists have noticed an absence of
depression in patients with severe traumatic brain injury, yet
cortisol is reduced below normal levels in those patients
(Reiter, 2005).
Is the persons brain really injured or is there another reason
for the assumed behavior? Is the brain injury still apparent?
What are the causes of the brain injury? These are the types of
diagnostic questions a neuropsychologist can answer
(www.neuropsychologycentral.com, 2002).
Brainstem Injuries and the Patient
An understanding of the anatomy of the brainstem helps identify
possible scenarios when treating patients with brain injury. The
brainstem consists of hindbrain, midbrain, and posterior central
structures of the forebrain (Kalat, 2004). In the medulla and
pons, reticular nuclei are important in adjusting heart rate,
respiration and blood pressure. The reticular formation of the
pons and midbrain is vital for the maintenance of consciousness.
It has been found that lesions in this area result in states of
coma (www.neuropsychologycentral.com, 2002). The reticular
nuclei are essential for arbitrating eye movement. Various
brainstem nuclei provide a key source of particular
neurotransmitters such as the locus coeruleus (norepinephrine),
the raphe nuclei (serotonin), and the substantia nigra
(dopamine). Reduction in norepinephrine or serotonin most likely
affects arousal and emotion (www.neuropsychologycentral.com,
2002). Research has suggested that Parkinsons disease is related
to loss of dopamine in the substantia nigra. Lesions of one
cerebellar cortex in the cerebellum result in ataxia on the same
side as the lesion (Landolfi.com, 2005).
Other common symptoms that the patient may encounter include
double vision, difficulty swallowing, weakness, unsteady gait,
drowsiness. Headaches, nausea and vomiting are usually due to
tectal lesions, while cervicomedullary lesions usually present
with dysphagia, unsteadiness, nasal speech, vomiting, and
weakness (Landolfi, 2005). Rarely, behavioral changes or
seizures may be seen in children. Older children may have
deterioration of handwriting and speech (Spencer, 2005). Lesions
in the pons are associated with any or all of the above
symptoms, depending on locality and extension. Midbrain and
lower brainstem/upper spinal cord signs and symptoms may be seen
with extension of the neoplasm to involve these structures
(Landolfi, 2005). Research has suggested that when infants and
children show signs of failure to thrive, glioma in the pons or
pontine glioma should be considered.
The patient with brainstem tumors may experience behavioral and
emotional changes, difficulty speaking and swallowing, hearing
loss, drowsiness, muscle weakness on one side of the face (e.g.,
tilting of the head), muscle weakness on one side of the body,
vomiting, drooping eyelid or double vision, and uncoordinated
gait (UFL, 2005). Research has shown that lesions in the
brainstem or cerebral hemisphere may cause horizontal gaze
palsy. If lesions occur below the crossing of the fibers from
the frontal eye fields in the caudal midbrain, will cause
weakness of gaze toward the side of the lesion (UFL, 2005).
Horizontal gaze palsy: Another way to remember this is that
patients with hemisphere lesions look toward their lesion, while
patients with pontine gaze palsies look away from their lesions
(Theodosopo ulos, 2005). Further, patients do not complain about
diplopia, or double vision, when afflicted with gaze palsy
because they still have conjugate eye movements.
Research has found that lesions of the medial longitudinal
fasciculus (MLF) between the sixth and third nerve nuclei cause
weakness of adduction on attempts at horizontal gaze, but not
with convergence (Theodosopoulos, 2005). For example, a lesion
of the right (MLF) will cause limitations of adduction of the
right eye on attempted leftward gaze. One can demonstrate that
this weakness is not caused by medial rectus paralysis, because
this muscle functions normally during convergence (which is
coordinated entirely in the midbrain) (Theodosopoulos, 2005).
Brainstem injury and the employer/ social worker
The employer or social worker benefits from the results of the
neuropsychologists evaluation of the afflicted persons.
Consultation helps employers and social workers understand the
capacity and limitations of said persons. It is with this
knowledge that a social worker can begin to understand the depth
of the situation at hand concerning brain injured persons. For
instance, an understanding of which brain functions are impaired
and which remain intact, can help direct decision making
concerning the social worker and employer. The employer and
social worker may want to know how the affected individual will
perform, think, and behave concerning work related duties. Will
the employee be able to concentrate on various tasks and for how
long? How do emotional or psychological factors influence
performance or concerns? Wh at conditions are necessary for him/
her? How competent is the employee? Do they need constant
attention? Is it safe for them to drive? What about managing
money? Can they ultimately return to work or school? Will the
therapy interfere with work/ school? All of these questions are
valid concerns. With the help of the neuropsychologist,
employer, and or social worker, the patient can have a much
better chance at a more successful return rate for work
depending on the severity of the damage done to the brainstem.
References
Halligan, Peter; Kischka, Udo; Marshall, John (2003).Handbook of
Neuropsychology. Oxford University Press Inc., New York. p.487.
Neuropsychologycentral web page (2002). Retrieved May 1, 2005
from
http//www.neuropsychologycentral.com/interface/content/resources
/resources_interface_frameset.html.
University of Florida (2005). Medical Informatics: Introduction
to Clinical Neurology. Retrieved May 1, 2005 from
http://medinfo.ufl.edu/year2/neuro/review/bsc.html.
Joseph Landolfi (2005). Brainstem Gliomas. Retrieved May 1, 2005
from http://www.emedicine.com/NEURO/topic40.htm.
Spencer, Rick (2005). Brain Injury 101. Retrieved May 1, 2005
from http://www.rickspencer.com/Headinjurylaw/brain101.htm.
Theodosopoulos, Philip; Burton, Lisa; Wagner, Becky;
Splitt, Nancee (2005). Retrieved May 1, 2005 from
http://www.mayfieldclinic.com/PE-BrainTumor.htm.
Reiter, Jamie (2003). Journey Toward Recovery: A Brain Injury
Guide For Families. Retrieved May 1, 2005 from
http://www.sdbif.org/Guide/SDBIF_Guide_Eng.pdf.
Jeff Slocum Professor Morgan
Brainstem Injuries and the Neurosurgeon, Neurologist, and
Spouse and other family members.
Cognitive Psychologists study the function of the normal
brain. Clinical NeuroPsychologists, guided by information
processing models of cognitive function, investigate patients
disabilities to find the defective component in their
information processing. They determine the anatomical location,
etiology, and treatment of the lesion and study the cognitive
consequences (Margolin, 1992).
Psychiatrists follow a protocol of what to examine and how,
based on standing theories of cognition. Their narrow rules of
diagnosis are based on research. This prevents using diagnosis
as a political weapon. Disabilities such as autism are
relatively refractory to intervention. Consequently the central
principle of treatment in such cases is to evaluate the symptoms
to determine the appropriate environment in which to manage the
patient. There is an ongoing effort to develop standardized
tests to quantify the otherwise soft data. For instance there is
an algorithm for interviewing family members to estimate risk of
suicide (Bebbington, 1991).
The family may provide the patient with moral support or opt
to wish the patient well and carry on with their own lives
(typical of adolescence) or a divorce might precede the
financial decimation of medical bills. The San Diego Brain
Injury Foundation says a supportive family should choose a
spokesperson that is good at communicating with medical
personnel and grasping scientific concepts. The organization
recommends knowing the names, roles, and phone numbers of the
various personnel. And they recommend researching the disorder.
This organization also delegates this task to the spokesperson.
They recommend keeping a diary including a detailed medical
history of the patient. (The author should take a course in
medical ethics!) The diary should contain all questions asked
of the me dical team and their answers. The author says the San
Diego Brain Injury Foundation will guide the search for
information on the patients injury and provide contact numbers
with similar survivors.
Damage to the brain stem can generate problems of attention,
concentration, sleep/wake cycles, consciousness, respiration,
and heart rate (Reiter, 2003).
The employer may hire a temporary help if the patient is
irreplaceable; or he may decide this is a good time to down-
size.
The first test in assessing the cognitive function of a
patient is always the Mini-mental Status Exam. It should take
all of three minutes. It tests:
1) the level of consciousness
2) attention,
3) orientation to person, place, and time;
4) language,
5) and memory.
The exam is hierarchical and must be done in a predetermined
order as some tests depend on the proper function of other areas
(i.e. comprehension is required to test praxis). Symptoms that
can result from a brainstem lesion are dysarthria, diplopia, and
facial numbness. This can result from herniation of the
brainstem (uncal herniation) from the middle to the posterior
cranial fossa, bruising the hippocampus and amygdala against the
firm tentorium (Devinsky, 1992).
Uncal herniation can result from post-traumatic hygroma. In the
elderly the trauma may be nothing more than a fall to the
floor. It used to be called hydroma for a collection of fluid
between the dura mater and the arachnoid membrane. It is
believed to result from a tear in the arachnoid membrane forming
a one-way flap that admits cerebrospinal fluid and trapping it.
The capillaries of the arachnoid rupture 58% of the time
transforming the fluid accumulation into a subdural hematoma.
Twenty eight percent of subdural hematoma patients die. The
hygroma is often left to resolve on its own if it does not get
large enough to herniate the brainstem. Eighty five per cent
will enlarge for one month and then regress over the next three
to four months. The symptoms that may result from the increased
intracranial pressure are confusion, decrea sed coordination,
weakness, and headache. Hygromas tend to occur in the extremes
of age: before ten years old and after fifty years of age
(Herold, 2004). The brainstem is the origin of the cranial
nerves. It is involved in memory and movement. The thalamus is
the dorsal end of the brainstem. All sensory, except olfaction,
passes through the thalamus en route to the cortex. Possible
brainstem problems are: diplopia (cranial nerves III, IV, & VI),
choking (cranial nerves V & IX), and dysarthria (IX & XII).
Classical conditioning occurs in the lateral interpositus
nucleus (LIP) of the cerebellum. In the midbrain portion of the
brainstem is the substancia nigra whose degeneration is
responsible for Parkinsons Disease (Kalat, 2004).
Herpes simplex can produce encephalitis that causes the brain
to swell, raising intracranial pressure. The pressure can be
great enough to require temporary removal of part of the skull
to relieve the pressure to prevent uncal herniation. Without
treatment 70% will die. Ninety per cent of survivors will have
permanent neurologic impairment. The symptoms of herpies
encephalitis are persistent headache and stiff neck (Yan, 2002).
Ischemic stroke can produce brain swelling and uncal
herniation. The most effective treatment of ischemic stroke is
surgical embolectomy to remove the clot. This has to be
completed within six hours after the onset of ischemia to save
the endangered tissue. Recanalization is successful in two
thirds of surgeries compared to thirteen per cent for
thrombolysis therapy with tissue plasminogen activator (TPA).
TPA is more effective if delivered to the clot by catheter. This
also enables a lower dose compared to systemic intravenous
therapy thus reducing the risk of hemorrhage. The symptoms of
hemispheric ischemia are stupor with hemiplegia and conjugate
deviation of the eyes toward the ischemic hemisphere (Touho,
1991).
An MRI study of patients with infarcts in various parts of
the Pons determined that the Pons are involved in REM sleep
based on the reduction of REM sleep by the patients. REM was
abolished in a cat with bilateral lesions to the nucleus
reticularis pontis oralis (Landau, 2005).
The second most common cause of age-related dementia is ischemia
due to vascular disease. More than half of the cases diagnosed
as due to subcortical ischemia involve brainstem infarcts
(Kalaria, 2004). Brainstem infarcts are one of the causes of
acute ocular mononeruopathy (trouble focusing both eyes on the
same target) (Chou, 2004).
One elderly patient developed sudden tinnitus and hearing loss
on the right side with vertigo and emesis. An MRI scan found
occlusion of the anterior inferior cerebellar artery had caused
infarction of the right lateral inferior pontine tegmentum (Lee,
2004).
Uni- or bilateral sudden deafness may result from
vertebrobasilar ischemia (VBI) which is usually associated with
vertigo (Lee, 2005). A stroke in the ventral Pons from an
obstructed basilar artery can result in the locked-in syndrome.
It is characterized by quadriplegia, an-arthria, lower cranial
nerve palsies, consciousness, and vertical gaze (New, 2005).
Depression is a frequent co-morbid factor in neurologic
disorders including strokes (Kanner, 2003). Half of all strokes
never produce a detectable change on CT scan. The scan is still
of use to limit the diagnosis by ruling-out tumors and
hemorrhages (Warlow, 2003).
References
Bebbington, P. (1991). Social Psychiatry. London: Transaction
Publishers.
Chou, K., Galetta, S., Grant, L., Volpe, N., Bennett, J.,
Asbury, A., & Balcer, L. (2004). Acute ocular motor
mononeuropathies. Journal of the Neurological Sciences, 219 (1-
2), 35-39.
Devinsky, O. (1992). Behavioral Neurology. St. Louis: Mosby-
Year Book Inc.
Kalaria, R., Kenny, R., Ballard, C., Perry, R., Ince, P., &
Polvikoski. (2004). Towards defining the neuropathological
substrates of vascular dementia. Journal of Neurological
Sciences, 226 (1-2), 75-80.
Kanner, A. M., & Barry, J. J. (2003), The impact of mood
disorders in neurological diseases. Epilepsy & Behavior, 4 (3),
3-13.
Herold, T., Taylor, S., Affrescia, K., & Hunter, C. (2004). Post
Traumatic Subdural Hygroma. Journal of Emergency Medicine, 27
(4), 361-366.
Kalat, J. (2004). Biological Psychology (8th ed.). Belmont, CA:
Wadsworth/Thompson Learning.
Landau, M., Maldonado, J., & Jabbari, B. (2005). The effects of
isolated brainstem lesions on human REM sleep. Sleep Medicine, 6
(1), 37-40.
Lee, H., Ahn, B., & Baloh, R. (2004). Sudden deafness with
vertigo as a sole manifestation of anterior inferior cerebellar
artery infarction. Journal of the Neurological Sciences, 222 (1-
2), 105-107.
Lee, H., & Baloh, R. W. (2005). Sudden deafness in
vertebrobasilar ischemia. Journal of the Neurological Sciences,
228 (1), 99-104.
Margolin, D. (1992). Cognitive NeuroPsychology. New York: O
xford University Press.
Thatnagar, S., & Mandybur, G. Effects of intralaminar thalamic
stimulation on language functions. Brain and Language, 92 (1),
1-11.
New, P. W., & Thomas, S. J. (2005). Cognitive impairments in the
locked-in syndrome. Archives of Physical Medicine and
Rehabilitation, 86 (2), 338-343.
Reiter, J., (2003) Retrieved May 4, 2005, from
http://www.sdbif.org/Guide/SDBIF_Guide_Eng.pdf.
Touho, H., Morisako, T., Hashimoto, Y., and Karasawa, J. (1991).
Surgical Neurology, 51 (3), 303-320.
Warlow, C., Dphil, C. S., Dennis, M., Wardlaw, J., & Sandercock,
P. (2003). Stroke. Lancet, 362 (9391), 1211-1224.
Yan, H. (2002). Herpes Simplex Encephalitis. Surgical
Neurology, 57 (1), 20-24.
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This page last edited 1-3, 2005
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