A subdural hemorrhage is more likely, due to the fact that there is no obvious fracture and the accident was about 18 hours ago. Subdural hematomas form when there is bleeding involving the dura mater and the brain. The patient presented with a mild headache the day after the bike accident where he obtained superficial lacerations on his forehead. Headache is a key symptom of subdural hemorrhage and given the location of the lacerations being the front of the skull, the patient could develop an acute subdural hematoma (MedlinePlus on Subdural Hematoma, 2019). Epidural hematomas are where there is bleeding involving the dura mater and the skull. Epidural hematomas are more severe and usually consist of a fractured skull (Huether & McCance, 2017).
The major concern at this time is possible brain herniation, due to the increased intracranial pressure which is life threatening. The symptoms of tiredness, confusion, and difficulty concentration can lead to the patient losing consciousness, dilated pupils, and respiration changes which are symptoms of herniation of the temporal lobe (Huether & McCance, 2017). Emergency surgery may be required to release the pressure in the brain. Blood clots can also be removed by a craniotomy procedure (MedlinePlus on Subdural Hematoma, 2019). Given the patients declining symptoms, the patient needs to be further assessed for increased intracranial pressure that can result in temporal lobe herniation.
The primary type of medication used to treat myasthenia gravis are cholinesterase inhibitors such as pyridostigmine and neostigmine, steroids such as prednisone, and immunosuppressant medications such as azathioprine and cyclosporine (Mayo Clinic: Myasthenia gravis). Myasthenia gravis is a disease that attacks acetylcholine receptors which results in the interruption of nerve impulses and declining depolarization of the muscles. Anticholinesterase medications improve nerve and muscle communication by preserving acetylcholine.
Acetylcholine is a neurotransmitter present in the sympathetic and parasympathetic nervous system (Huether & McCance, 2017). Cholinesterase inhibitors or anticholinesterase medications stop the breakdown of acetylcholine at the neuromuscular junction, thereby increasing muscle strength and controlling contractions. Steroids can decrease the production of antibodies that obstruct acetylcholine. Immunosuppressants can also be used to help the autoimmune disease (Mayo Clinic: Myasthenia gravis, 2019). These medications can assist in improving the symptoms of myasthenia gravis.
The components of Alzheimer’s disease consist of the development of neurofibrillary tangles and senile plaques (Perry, Avila, Zhu, & Kehoe, 2018). Throughout the years, many theories have been constructed regarding the pathogenesis of Alzheimer’s disease, such as the cholinergic hypothesis and the amyloid cascade hypothesis. In the cholinergic hypothesis, decline in cognition is thought to be related to the decline of acetylcholine which is a neurotransmitter in the central nervous system. The acetylcholine decline directly impacts choline acetyltransferase which results in loss of nicotinic and muscarinic acetylcholine receptors.
The medications used to treat Alzheimer’s disease can stop the breakdown of acetylcholine, but the medications are not able to prevent the progressive and debilitating disease. On the other hand, the amyloid cascade hypothesis states the effect of the AB peptide on the brain relating to the occurrence of disproportionate levels causing the development of Alzheimer’s. A new hypothesis has developed and believes that the renin angiotensin system is altered in patients who have cardiovascular disease making them more prone to the development of Alzheimer’s disease. Studies have also shown a connection with angiotensin-converting enzyme (ACE) and the development of Alzheimer’s at an early age. Data has displayed that ACE can cause a decline of B- amyloid peptide (AB) (Perry et al., 2018).
Two other conditions that may present similarly to Alzheimer’s disease, but would be treated differently and have potentially different outcomes are delirium and trauma to the head. Delirium can present with symptoms that are similar to Alzheimer’s, such as disorientation and confusion. Delirium can be caused after a surgical procedure or can be due to various medications and the onset is rather fast. Once the cause of delirium is discovered and treated, mental cognition will improve back to the patient’s baseline.
Some other causes of delirium can be alcohol withdrawal and/or infection. To differentiate Alzheimer’s from delirium, the patient’s history, presenting symptoms, as well as laboratory tests should be considered. Alzheimer’s is a slow progression disease and irreversible whereas delirium can occur rather rapidly and is reversible (Ellison, 2018). Head trauma can display similar symptoms to Alzheimer’s and can cause decline of cognition. Imaging tests such as CT scans and MRI can be utilized to see if there is a hematoma, hemorrhage, or contusion of the brain. Treatment for head trauma is based on how severe the injury is (Mayo Clinic, 2019).
Two other diseases that can present similarly to Alzheimer’s disease, but would be treated differently and have different outcomes are Lewy Body Dementia and Huntington’s Disease. Lewy Body Dementia can present like Alzheimer’s disease and is related to the development of Lewy bodies in the brain. Some key symptoms present in Lewy body dementia are movement symptoms, hallucinations, and malfunctions of the autonomic nervous system causing falls and incontinence of urine. Memory loss can also occur but is seen more in Alzheimer’s.
There is no prominent cause of Lewy body dementia and no cure to stop the cells in the brain from being damaged by the Lewy bodies (Alzheimer’s association: Lewy Body Dementia, 2019). Huntington’s disease can cause symptoms that are similar to Alzheimer’s disease. Huntington’s disease is caused by a dominant genetic defect on chromosome 4 gene which causes the huntingtin protein to be defective. Huntington’s disease can cause movements that are involuntary, loss of thinking skills, and decline of memory. A genetic test can be conducted to diagnosis Huntington’s disease, but there is no cure to reverse the defect that affects the brain (Alzheimer’s association: Huntington’s Disease, 2019).