Brainstem Lesions Symptoms

Mainly lower extremity weakness and sensory loss, and to a lesser extent, arm weakness and sensory loss

Toward the lesion

Contralateral weakness and sensory loss

Mainly the lower extremity

To a lesser extent

The two main hypotheses for the pathophysiology of diabetic neuropathy are the vascular hypothesis and the metabolic hypothesis. The vascular hypothesis suggests that occlusion of the vasa nervorum leads to neuropathy, while the metabolic hypothesis proposes that hyperglycemia leads to the accumulation of glycosylation end products, increased formation of sorbitol and fructose in Schwann cells, and increased reactive oxygen species, ultimately causing neuronal damage.

The clinical features of chronic, progressive diabetic neuropathy include symmetric, distal sensory loss, with early stage symptoms involving loss of vibration, pain (deep before superficial), and temperature sensation.

The two main types of inherited polyneuropathies mentioned in the passage are neuropathy with mitochondrial diseases and recurrent or relapsing polyneuropathies such as porphyria and CIDP.

Early chronic sensorimotor polyneuropathy (months to a year or two) is typically seen in conditions like diabetes, CIDP, and uremia, while late chronic sensorimotor polyneuropathy (years to decades) is associated with inherited polyneuropathies.

Subacute peripheral nerve disorders occur over weeks to months and are often due to nutritional deficiencies, toxins, or neoplastic/granulomatous infiltration, while chronic peripheral nerve disorders can be early (months to a year or two) or late (years to decades) and are often due to conditions like diabetes, CIDP, or inherited polyneuropathies.

Sensorimotor paralysis is a subacute (weeks to months) condition, while sensorimotor polyneuropathy can be an early chronic (months to a year or two) or late chronic (years to decades) condition. Sensorimotor paralysis is often due to nutritional deficiencies, toxins, or neoplastic/granulomatous infiltration, while sensorimotor polyneuropathy is associated with conditions like diabetes, CIDP, uremia, and inherited polyneuropathies.

Myasthenic crisis is an acute, life-threatening exacerbation of myasthenic symptoms that can lead to respiratory failure. Risk factors include physiologic stress like infection, surgery, anesthesia, pregnancy, and stress, as well as certain medications like aminoglycosides, muscle relaxants, and benzodiazepines.

Common signs and symptoms of a myasthenic crisis include muscle weakness, dyspnea, sweating, agitation, disorientation, drowsiness, and urinary and fecal urgency. Additionally, patients may present with normal pupils, tachycardia, and no fasciculations.

In a myasthenic crisis, early intubation should be considered if there is a risk of respiratory failure. It is essential to perform spirometry and respiratory muscle function tests before deciding to intubate. Pharmacotherapy should be initiated with specialist guidance.

Immunomodulants and biological agents such as Rituximab and Eculizumab are used in the treatment of thymoma or failure of medical therapy.

Physiological stressors like infection, surgery, anesthesia, pregnancy, and stress, along with medications such as aminoglycosides, muscle relaxants, and benzodiazepines, are risk factors for myasthenic crisis.

It has a tonic phase with generalized muscle contractions (rotated eyes, apnea, lateral tongue biting, etc.) followed by a clonic phase with rhythmic muscle twitching.

Confusion, amnesia of the event, drowsiness, hypersalivation.

There is a sudden loss of muscle tone, leading to a sudden head drop or collapse, lasting less than 15 seconds.

Interrupted motion or activity, blank stare, unresponsiveness that can occur multiple times a day, along with subtle automatisms like lip-smacking or eye fluttering.

Focal seizures can occur with loss of awareness, while generalized seizures can occur without obvious loss of consciousness.

Triggers like hyperventilation or flashing lights, along with postictal symptoms like amnesia, confusion, or drowsiness after an event.

The most common type of lacunar stroke (>50%) is a stroke affecting the posterior limb of the internal capsule, causing contralateral hemiparesis of the face, arm, and leg (leading to circumduction gait), and in some cases, dysarthria. However, there is no sensory impairment.

Wallenberg syndrome is characterized by ipsilateral symptoms like nausea, vomiting, dizziness, vertigo, tinnitus, diplopia, dysconjugate gaze palsy, Horner syndrome, and uncontrollable hiccups, as well as contralateral symptoms like hemiplegia or quadriplegia, sensory loss of the hemi-body and all four limbs, and a cross sign (lesion in brainstem affecting CN ipsilaterally and spinal tract contralaterally).

An AICA stroke is characterized by ipsilateral gait and limb ataxia, palsies of cranial nerves V, VII, and VIII (causing ipsilateral loss of facial sensation to pain and temperature, facial muscle weakness, decreased lacrimation and salivation, loss of taste sensation from anterior ⅔ of the tongue, vertigo, nystagmus, and hearing loss), and ipsilateral Horner syndrome, as well as contralateral loss of pain and temperature sensation.

A SCA stroke is characterized by dysarthria and limb ataxia.

A basilar artery stroke (basilar syndrome) is characterized by somnolence, vivid hallucinations, dreamlike behavior, and cranial nerve III dysfunction, as well as ipsilateral symptoms like ataxia, diplopia, dysphagia, dysarthria, and vertigo, and contralateral homonymous hemianopsia.

In supratentorial infarction, the eye is deviated toward the affected side (ipsilateral). In infratentorial infarction, the eye is deviated away from the affected side (contralateral). In epilepsy, the eye is also deviated away from the affected side (contralateral).