Pamantasan ng Lungsod ng Maynila College of Medicine Department of Internal Medicine
RELOJ, JERNELYN P. Medicine III-B 19 January 2007 Case 1 – A case of stroke This is a case of Mrs. MM, a 75-year old female patient, right-handed, diabetic and hypertensive, from Tondo, admitted for the first time in a tertiary hospital in Manila. She was brought to the hospital because of sudden-onset paralysis of the right arm and leg. Patient’s condition started six hours prior to admission, when she experienced numbness and feeling of heaviness of her right arm and leg upon waking up in the morning of her admission date. She was still able to rise from her bed, until about 4 hours prior, she noted worsening of her condition, such that she can no longer move her right arm and leg. She denied having headache, dizziness, nor episodes of vomiting. Two hours prior, her relatives noticed that her face appeared asymmetrical and the patient has “difficulty talking”. Subsequently, she was rushed to the medical facilities. Patient had a variety of medical illnesses for the past several years. She was diagnosed to be hypertensive, with highest BP at 180/100 mmHg and usual BP of 160/90 mmHg; poorly compliant to Metoprolol 100 mg tabs. Likewise, Metformine 500 mg is being taken irregularly for her blood sugar. For the past 6 months, she has been experiencing mild numbness of her right extremities and episodes of slurred speech, however, these episodes would subside after few hours of rest and intake of antihypertensives. General PE revealed an obese elderly patient, bed-ridden, with the following vital signs: BP = 170/90 mmHg (both arms); CAR = 98 bpm (irregular); RR = 19 cpm. There is decreased carotid pulsations at the right, with a soft bruit on the left carotid area in the neck. Chest and lung findings are unremarkable. Her PMI is displaced laterally, no heaves, with an irregular cardiac rhythm. Peripheral pulses are equal. Neurological findings revealed an awake patient, she can follow simple commands (eg. Raising her left arm), but is unable to respond verbally to questionings. There are attempts to talk, but she can’t respond verbally to questions, there are efforts to communicate by gestures. Cranial nerve findings: Pupils are equally reactive to directly and consensually Fundi: no pailledema, with grade I hypertensive retinopathy With slight preferential gaze to the left, no gross EOM paralysis With right central facial paralysis Intact pharyngeal reflex Tongue deviated to the right on protrusion She has 0/5 MRC muscle strength grade on her right arm and leg; with 5/5 MRC on the left extremities. Sensory testing cannot be reliably tested due to patient’s inability to respond verbally, though there appear to be less withdrawal responses of the right arm and leg when painfully stimulated. There is hypoflexia on her right arm and leg with (++) responses on the left. No signs of meningeal irritation; with dorsiflexion plantar response on the right. Student’s Tasks: 1. Summarize all the neurological findings and make a clinicoanatomic correlation (Neurological Localization) 2. Based on the temporal profile, make an initial impression. Cite and justify at least 3 differential diagnoses. 3. Make a diagnostic plan to come up with a clinical diagnosis. 4. Discuss the immediate and long-term interventional plans for this patient.
I. Neurological Findings in the Patient Numbness and feeling of heaviness in the right arm and leg Sudden onset paralysis of the right arm and leg Right central facial paralysis Dysarthria Can follow simple commands and communicates with gestures Slight preferential gaze to the left, no EOM paralysis Tongue deviated to the right on protrusion Intact pharyngeal reflex 0/5 MRC muscle strength grade on right arm and leg Less withdrawal responses of the right arm and leg on painful stimuli Hypoflexia on the right arm and leg Babinski’s sign/Dorsiflexion plantar response on the right
This is a tabulation of the neurologic findings in the patient and the part of the nervous system that could be involved or responsible for the finding: Neurologic Finding Localization Numbness and feeling of heaviness in the right arm Primary motor area? and leg Corticospinal tract? Lower motor neuron? Peripheral nerves? NMJ? Muscles? Sudden onset paralysis of the right arm and leg Primary motor area? Corticospinal tract? Lower motor neuron? Peripheral nerves? NMJ? Muscles? Right central facial paralysis Primary motor area? Corticobulbar tract? CN VII nucleus in the brainstem? CN VII peripheral course? NMJ? Muscles? Dysarthria Corticobulbar tract? CN V, VII, IX, X, XII nucleus in the brainstem? Peripheral courses of the CN? NMJ? Can follow simple commands and communicates Unaffected higher cortical functions with gestures Intact mental functioning Slight preferential gaze to the left, no EOM CN III? paralysis CN VI? Tongue deviated to the right on protrusion CN XII? Intact pharyngeal reflex Unaffected CN IX 0/5 MRC muscle strength grade on right arm and Primary motor area? leg (hypotonia) Corticospinal tract? Lower motor neuron? Peripheral nerves? NMJ? Muscles? Less withdrawal responses of the right arm and leg Spinothalamic tract? on painful stimuli Spinoreticular tract? Peripheral nerves?
Hypoflexia on the right arm and leg
Babinski’s sign/Dorsiflexion plantar response on the right
Primary motor area? Corticospinal tract? Lower motor neuron? Peripheral nerves? Upper motor neuron? Peripheral nerve? NMJ? Muscles?
The numbness in the right arm and leg which had suddenly progressed to paralysis could be a manifestation of a lesion involving the primary motor area or the Brodmann’s area 4 of the cerebral cortex. This is further strengthened by the fact that lesions in this area also bring about hypotonia, hypoflexia, and Babinski’s sign – all of which are manifested by the patient. However, in lesions involving the primary motor region, Babinski’s sign only occurs after a few weeks time, together with the development of spasticity of the affected musculature and enhanced muscle stretch reflexes. This is not the case of the patient. Babinski’s sign developed few hours after the occurrence of paresis.
The peripheral nerves are unlikely to be involved. Injury of an individual peripheral nerve is followed by paralysis of muscles and loss of sensation distal to the lesion, involving only muscles and skin areas supplied by the injured nerve. The paralyzed muscles are flaccid and gradually undergo severe atrophy. All forms of sensation, including proprioception are lost. Clearly, this is not the case of the patient. As the history implies, the paralysis is diffused in the right side of her body and she still responds to painful stimuli. Polyneuropathy is also unlikely, because in this disease, the lesions often occur bilaterally and the symptoms occur in glove-and-stocking distribution. The patient did not manifest any of these. The lower motor neurons might be involved. Lower motor neurons are the anterior horn cells of the spinal cord, which innervate the skeletal muscles of the body, and the motor nerve cells of the brainstem, which innervate muscles supplied by the cranial nerves. Lesions in these neurons abolish both the voluntary and reflex responses of muscles. In addition to paralysis, the affected muscles show hypotonia and absence of the muscle stretch reflexes. These symptoms are manifested by the patient. However, in lesions involving the LMNs, the muscles would then show atrophy together with fibrillations and fasciculations. These are not seen in the patient, hence, LMNs are unlikely to be involved. In the case of the patient, the corticospinal tract (pyramidal tract), the pathway primarily concerned with skilled movements of the distal muscles, could be involved. The corticospinal (pyramidal) tract consists of upper motor neurons in the cerebral cortex with axons coursing through the pyramidal tract in the medulla and terminating on anterior horn cells or interneurons in the spinal cord.
A few weeks after the onset of these early manifestations, lower motor neuron lesions would display muscle atrophy, fibrillations, and fasciculations. Although, these symptoms are not seen in the patient, I cannot rule out involvement of the LMNs yet. As what is previously stated, these later manifestations would occur only after a few-week time, and the patient has only been experiencing the manifestations for some hours.
What about the occasional numbness and slurred speech? Given the aforementioned neurologic findings, it can be concluded that the primary motor region in the cerebral cortex can be involved. This region in the supratentotial level, also called the Brodmann’s area 4 is where the motor system of the body originates. The primary motor cortex is organized into columns of neurons, to which, each column is a functional entity responsible for directing a group of muscles acting on a single joint. With this organization, movements, not individual muscles, are represented in the motor cortex. True enough, lesions in the primary motor region result immediately in
paresis of the contralateral musculature with hypotonia and diminished muscle stretch reflexes. These would then lead to development of spasticity of the affected musculature, and enhanced muscle stretch reflexes, and Babinski’s sign. These findings are synonymous with the manifestations presented by the patient. However, if the cerebral cortex is involved, the typical sensory finding is that there is contralateral sensory loss on the limbs and trunk on the same side as the motor deficits. The patient did not have any loss of sensation, hence, involvement of this area could be disregarded. However, if the cerebral cortex is involved, the typical sensory finding is that there is contralateral sensory loss on the limbs and trunk on the same side as the motor deficits. The patient did not have any loss of sensation, hence, involvement of this area could be disregarded. The aforementioned localization points to a lesion, along the corticospinal tract, as the one responsible for the manifestations of the patient. As we know, the corticospinal tract originates in the cortex, passes through the internal capsule, courses through the brainstem (midbrain, pons, and medulla), then decussates, and ends up synapsing with the anterior horn cells of the spinal cord. Where within this pathway could the lesion be is the question. As stated before, the origin of the corticospinal tract is the cerebral cortex, specifically the primary motor area. Lesions in the primary motor region result immediately to paralysis of the face, arm, and leg (hemiplegia) of the opposite side of the body, with hypotonia, and depression of the muscle stretch reflexes. These would then lead to development of spasticity of the affected musculature, and enhanced muscle stretch reflexes, and Babinski’s sign. These findings are synonymous with the manifestations presented by the patient. The corticospinal tract then courses through the internal capsule. A lesion in the posterior limb of the internal capsule would also manifest as that a lesion in the primary motor area. However, taking into account the other symptoms presented by the patient – dysarthria, gaze preference to the left side, tongue deviation upon protrusion to the right side – more likely, there are cranial nerve involvement, which directs me to think of a lesion in the level of the brainstem.