CLINICAL CASE #3
A 59-year-old, right handed male was admitted to the hospital with a chief complaint of
occipital headaches of 3 weeks’ duration. The patient had been under treatment for
hypertension for 2 years. Two weeks prior to admission, the patient noted a sudden onset
of diploplia [i.e., double vision] on forward gaze and a sensation of dizziness. One
day prior to admission he noted a relatively sudden onset of ptosis (drooping) of the
right eyelid.
The patient was a well-nourished man of medium height who appeared his stated age.
Funduscopic examination revealed clear optic disc with sharp borders. [This means that
eh patient didn’t have “pappiledema”, a swelling and reddening of the optic nerve head
that may indicate increased intracranial pressure]. His skin was warm and of normal
texture. Blood pressure was elevated.
The patient was alert, cooperative, and oriented with respect to person, place, and time.
Memory was appropriate for his age. Speech was articulate and meaningful. Extraocular
movements were full, but the patient complained of diploplia. Nystagmus was
present on left lateral gaze. The right pupil measured 3mm, the left was 5mm, but
both responded to light and accommodation. Ptosis (drooping) of the eyelid and
decreased sweating on the right side of the face (anhidrosis) were also present.
Hearing was diminished in both ears to high frequencies. Pain, but not touch
sensation, was decreased on the right side of the face. The right corneal reflex was
diminished. Facial expressions were full and symmetric. The uvula deviated to the left,
and there was deficient elevation of the right side of the palate; there was also a
suggestion of hoarseness.
Strength was intact throughout the body; deep tendon reflexes were intact and symmetric.
An ataxia was evident in the right upper extremity on finger tapping, hand-patting,
and finger-to-nose tests. A side-to-side intention tremor was present. Ataxia was also
present in the right lower extremity on heel-to-shin and tibia-tapping tests.
There was decreased sensation to pinprick on the left side of the body, the left arm,
and the left leg. The patient was unable to distinguish between hot and cold on the
left side. Position, vibration, and touch modalities were intact throughout the entire body.
Discussion:
Please refer to http://www.neuroexam.com/ for videos of clinical tests:
Key Symptoms:
Cerebellar Signs:
- Right upper extremity ataxia
- Intention Tremor (Resting tremors are related to Parkinson while intention
tremors are cerebellar signs)
Remember: Ataxia is ipsilateral to the cerebellar lesion.
These symptoms can arise because of cerebellar hemisphere injury or injury leading to
interruption of input or output pathways (cerebellar peduncles).
Therefore this patient exhibits signs of right cerebellar damage.
Spinothalamic tract signs:
- Decreased sensation to pain and temperature involving the whole left side of
body.
Cranial Nerves Signs:
- CN V: Right loss of pain and temperature. Remember: pain and temperature
information from CN V is relayed to the spinal trigeminal nucleus and tract on
the same side of the body.
Right corneal reflex deficit is also due to damage of CN V. The corneal reflex
afferent is relayed by the pain fibers of the trigeminal system innervatin the eyes;
the efferent (blinking response) side of the reflex is relayed by CN VII. Because
the patient showed no indication of facial nerve damage, the problem is by
exclusion related to CN V damage.
- CN VIII: Vertigo, Nystagmus, Dizziness. Possibly hearing loss but the hearing
loss might be due to old age (it is hard to tell).
- CN X: Uvula and soft palate are innervated by CNX fibers originating from
Nucleus Ambiguus. Remember: Uvula deviates away from the lesion!
Therefore damage is to right CNX. Hoarseness is related to CN X damage too
because CN X is important to laryngeal voice muscles.
Sympathetic Signs:
Drooping of the eye lid, lack of sweating, and a small pupil together on the same
side of the body is a sign of sympathetic system damage to that side. This
constellation of symptoms is called Horner’s Syndrome (you don’t need to know
the name)
Although ptosis is usually caused by damage to CNIII, the sympathetic system
also innervates a muscle important for eye-lid opening (Mueller muscle). CNIII
damage will cause parasympathetic system signs and that will lead to ptosis of
the eye along with a bigger pupil which is opposite to what is being reported by
this patient.
2. Is the lesion inside or outside the CNS?
The patient suffers, among other things, from alternating hemiplegia: he exhibits cranial
nerve signs on the right and anterolateral signs (lack of pain and temperature sensation on the
left). This is a sure sign that the disease is in the CNS.
3. Is the lesion in the spinal cord or the brain?
The presence of cranial nerve signs is a sign of damage at a level higher than the spinal
cord.
4. Is the damage in the forebrain or brainstem?
Damage to cerebellum, CNV (spinal nucleus and tract), CNVIII, and CNX (nucleus
ambiguous) all point to a brainstem origin for the damage. More specifically, all the
affected cranial nerves are in the medulla.
The spinal trigeminal nucleus, nucleus ambiguous, and CNVIII are located in the lateral
medulla at the level of the inferior cerebellar peduncle. Also in the lateral medulla one
can find the anterolateral system conveying pain and temperature information from the
contralateral upper and lower extremities. Also in the same region one finds the
descending sympathetic tract.
Therefore all the symptoms can be explained by damage to one area of the brainstem in
lateral medulla region. The figure below shows a picture of the damage in this situation.
The lateral medulla syndrome is also know as Wallenberg syndrome and consists of the
following:
- Ipsilateral Horner syndrome (sympathetic damage)
- Ipsilateral atexia, nausea, vertigo.
- Contralateral loss of pain and temperature sensation in the body
- Ipsilateral loss of pain and temperature in the face
- Hoarseness and pharyngeal muscles issues
This patient has a right lateral medulla lesion.
5. What artery supplies this area?
PICA branch of the vertebral artery. This patient most probably had a PICA stroke.