NURS 6501: Week 7 Quiz:
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Question 1
A 45-year-old male presents with asymmetrical sensory loss and motor weakness following a traumatic spinal cord injury. Upon examination, he demonstrates ipsilateral loss of motor function and proprioception, along with contralateral loss of pain and temperature sensation below the level of the lesion. Which of the following best explains these clinical findings?
Group of answer choices
- Posterior cord syndrome affecting dorsal columns and leading to loss of proprioception and fine touch
- Anterior cord syndrome resulting in loss of motor function and pain/temperature sensation
- Central cord syndrome causing bilateral motor and sensory loss
- Brown-Séquard syndrome leading to ipsilateral loss of motor function and proprioception, and contralateral loss of pain and temperature sensation
- Ipsilateral (same side as lesion):
- Loss of motor function (due to corticospinal tract damage)
- Loss of proprioception, vibration, and fine touch (due to dorsal column involvement)
- Contralateral (opposite side of lesion):
- Loss of pain and temperature sensation (due to spinothalamic tract crossing within a few levels of entry)
- Posterior cord syndrome: Affects proprioception and fine touch only (dorsal columns), but motor function is preserved
- Anterior cord syndrome: Causes bilateral loss of motor and pain/temp, sparing dorsal column modalities (proprioception/fine touch)
- Central cord syndrome: Often presents with greater motor loss in upper limbs than lower, and sparing of proprioception
- Transverse myelitis
- Acute disseminated encephalomyelitis (ADEM)
- Optic neuritis
- Multiple sclerosis
- Monophasic (single episode, not relapsing)
- Widespread CNS demyelination
- Often follows a preceding infection or immunization
- Symptoms: encephalopathy, seizures, motor/sensory deficits, ataxia, etc.
- MRI shows diffuse, bilateral, asymmetric white matter lesions
- Transverse myelitis → Inflammation of the spinal cord, may occur as part of a monophasic or multiphasic disorder, but not disseminated across the CNS
- Optic neuritis → Inflammation of the optic nerve; typically focal, and often associated with multiple sclerosis
- Multiple sclerosis (MS) → Chronic, relapsing-remitting or progressive, disseminated CNS disorder — not monophasic
- Reduced serotonin levels causing vasoconstriction of cerebral blood vessels
- Excessive production of cerebrospinal fluid causing increased intracranial pressure
- Dysregulation of the hypothalamus leading to cyclical activation of the trigeminal-autonomic reflex
- Compression of the optic nerve due to an orbital mass
- Severe, unilateral periorbital pain
- Occurs in clusters (same time daily, often at night)
- Associated autonomic symptoms:
- Tearing (lacrimation)
- Nasal congestion or rhinorrhea
- Conjunctival injection (red eye)
- Ptosis or miosis (sometimes)
- Thought to involve the posterior hypothalamus, which regulates circadian rhythms.
- Dysregulation leads to cyclical activation of the trigeminal-autonomic reflex, which causes:
- Pain via trigeminal nerve activation
- Autonomic symptoms via parasympathetic outflow
- Reduced serotonin levels causing vasoconstriction → More related to migraine pathophysiology, not cluster headaches.
- Excessive CSF production → Would cause increased intracranial pressure, typically with diffuse headaches, not cyclical and unilateral.
- Compression of the optic nerve → Would result in visual deficits, not typical headache features with autonomic symptoms.
- Compression of cranial nerves by a brain tumor
- Spreading cortical depression and cortical spreading activation
- Chronic hypertension leading to cerebral ischemia
- Autoimmune-mediated demyelination of CNS neurons
- Unilateral throbbing headache
- Visual aura (flashing lights, blind spots)
- Nausea, vomiting
- Photophobia and phonophobia
- Triggered by stress, sleep disturbance, etc.
- Positive family history (migraines often run in families)
- Involves a phenomenon called cortical spreading depression (CSD):
- A wave of neuronal and glial depolarization that slowly propagates across the cerebral cortex.
- This leads to transient disruption in brain activity, causing aura symptoms.
- Followed by activation of the trigeminovascular system, resulting in inflammation, vasodilation, and pain.
- Compression of cranial nerves by a brain tumor → Would present with progressive neurological deficits, not episodic migraine-like symptoms.
- Chronic hypertension leading to cerebral ischemia → Causes vascular damage or stroke, not episodic migraines with aura.
- Autoimmune-mediated demyelination of CNS neurons → Seen in multiple sclerosis, which can sometimes cause headaches, but doesn’t match this classic migraine pattern.
- Chronic irritation of pain receptors at the injury site
- Localized inflammation spreading to nearby nerves
- Direct injury to adjacent tissues
- Cross-activation of nerve fibers in the spinal cord leading to pain perception in an area distant from the injury
- Sensory (afferent) fibers from different parts of the body (e.g., skin and internal organs) converge on the same second-order neurons in the spinal cord or brainstem.
- The brain may misinterpret the source of pain because it is more accustomed to receiving sensory input from somatic (surface) structures, rather than from visceral (internal) organs.
- Chronic irritation of pain receptors at the injury site → Explains localized chronic pain, not referred pain.
- Localized inflammation spreading to nearby nerves → Could lead to radiating pain, but not true referred pain.
- Direct injury to adjacent tissues → Causes local pain, not pain perceived in a distant site.
- Pain intensity is directly proportional to the extent of tissue damage
- Pain perception is unaffected by psychological factors
- Pain signals bypass the central nervous system and directly affect the brain
- Pain perception can be modulated by non-painful stimuli through inhibitory mechanisms in the spinal cord
- The spinal cord contains a "gate" mechanism in the dorsal horn that can either allow or inhibit pain signals before they reach the brain.
- Non-painful stimuli, such as touch, pressure, or vibration, can close the gate, thereby reducing the perception of pain.
- For example, rubbing a bumped elbow can reduce the pain because the touch fibers (A-beta fibers) activate inhibitory interneurons that "close the gate" on pain fibers (C fibers and A-delta fibers).
- Pain intensity is directly proportional to the extent of tissue damage ❌ Not always true; minor injuries can cause severe pain, and major injuries can sometimes cause little pain.
- Pain perception is unaffected by psychological factors ❌ Psychological factors (e.g. attention, emotion, context) play a major role in how pain is perceived.
- Pain signals bypass the CNS and directly affect the brain ❌ Pain signals are processed in the spinal cord and brainstem before reaching the brain’s pain centers.
- Apraxia
- Aphasia
- Alexia
- Agraphia
- Difficulty speaking
- Difficulty understanding spoken language
- No motor deficits
- Aphasia → Loss or impairment of language abilities (speaking, understanding, reading, or writing), typically due to a lesion in the dominant hemisphere, most often the left cerebral hemisphere (e.g., Broca’s or Wernicke’s area).
- Apraxia → Inability to perform purposeful movements, despite intact motor and sensory function.
- Alexia → Inability to read due to brain injury, often associated with damage to the left occipital lobe or angular gyrus.
- Agraphia → Inability to write, which may occur independently or alongside alexia or aphasia.
- Localization of the headache implies the tumor's location.
- The onset of the headache is usually sudden.
- Each tumor has a classic headache syndrome.
- The headache is typically worse in the morning.
- Increased intracranial pressure (ICP), which builds up overnight when the patient is lying down.
- As a result, the headache is often worse in the morning and may improve as the day goes on and the patient assumes an upright posture (which helps reduce ICP).
- Localization of the headache implies the tumor's location ❌ Not always true. Headache from increased ICP is often diffuse, and location does not reliably localize the tumor.
- The onset of the headache is usually sudden ❌ Tumor-related headaches typically have a gradual onset, not sudden like in subarachnoid hemorrhage or stroke.
- Each tumor has a classic headache syndrome ❌ There is no specific headache pattern that uniquely identifies a tumor type. Symptoms vary widely.
- Worse in the morning
- Wakes patient from sleep
- Associated with nausea/vomiting
- Progressively worsening over time
- Occipital lobe
- Frontal lobe
- Medulla oblongata
- Temporal lobe
- The hippocampus
- The entorhinal cortex
- Temporal lobe ✅ ✔ First affected (especially hippocampus) → causes memory loss.
- Occipital lobe ❌ ✘ Involved much later; associated with visual processing.
- Frontal lobe ❌ ✘ Affected in later stages; responsible for executive function and personality.
- Medulla oblongata ❌ ✘ Controls basic life functions (e.g., breathing, heart rate) and is not primarily involved in Alzheimer’s.
- Awareness/consciousness is maintained
- Automatisms, like lip-smacking
- Postictal confusion
- Tingling sensations in the extremities
- Loss of consciousness at onset
- A tonic phase (sustained muscle contraction)
- Followed by a clonic phase (rhythmic jerking)
- Confusion
- Fatigue
- Headache
- Sometimes amnesia for the event
- Awareness/consciousness is maintained ❌ → This is not true for generalized tonic-clonic seizures. Consciousness is lost.
- Automatisms, like lip-smacking ❌ → Seen in focal seizures with impaired awareness (formerly complex partial seizures), not tonic-clonic.
- Tingling sensations in the extremities ❌ → These are sensory auras, often seen in focal seizures, particularly from the parietal lobe.