According to Daniel Forbes writing for slate.com, the relative strength of modern strains are likely skewed because undue weight is given to much more expensive and potent, but less prevalent, samples. Some suggest that results are skewed by older testing methods that included low-THC-content plant material such as leaves in the samples, which are excluded in contemporary tests. Others believe that modern strains actually are significantly more potent than older ones. Price
The price or street value of cannabis varies widely depending on geographic area and potency. Prices and overall markets have also varied considerably over time. In 1997, cannabis was estimated to be overall the number four value crop in the US, and number one or two in many states, including California, New York, and Florida. This estimate is based on a value to growers of ~60% of retail value, or $3,000 per pound ($6,600/kg). In 2006, cannabis was estimated to have been a $36 billion market. This estimate has been challenged as exaggerated. The UN World Drug Report (2008) estimated that 2006 street prices in the US and Canada ranged from about US$8.8 to $25 per gram (approximately $250 to $700 per ounce), depending on quality. Typical U.S. retail prices were $10–15 per gram (approximately $280–420 per ounce). In 2017, the U.S. was estimated to constitute 90% of the worldwide $9.5 billion legal trade in cannabis.After some U.S. states legalized cannabis, street prices began to drop.
In rare cases, the patient might also experience muscle weakness, tremor, or paralysis if the nerves involved also control muscle movement. Pathophysiology
Postherpetic neuralgia is thought to be due to nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months, years, or for life.A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia neurons. Injury to sensory nerves induces neurochemical, physiological, and anatomical modifications to afferent and central neurons, such as afferent terminal sprouting and inhibitory interneuron loss. Following nerve damage, NaCl channel accumulation causes hyperexcitability, and downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) and TRPV1 channels. These changes contribute to increased NMDA glutamate receptor-dependent excitability of spinal dorsal horn neurons and are restricted to the ipsilateral (injured) side. A combination of these factors could contribute to the neuropathic pain state of postherpetic neuralgia. Diagnosis
Lab Studies:
No laboratory work is usually necessary. Results of cerebrospinal fluid evaluation are abnormal in 61%. Pleocytosis is observed in 46%, elevated protein in 26%, and VZV DNA in 22%. These findings are not predictive of the clinical course of postherpetic neuralgia. Viral culture or immunofluorescence staining may be used to differentiate herpes simplex from herpes zoster in cases that are difficult to distinguish clinically. Antibodies to herpes zoster can be measured.